United Statei Environ mental Criteria and EPA-6O0/8-83-028A
Environmental Protection Aaeeaament Office October 1983
Agency Reeaarch Triangle Park NC 27711 External Review Draft
Research and Development
Air Quality Review
Griteria for Lead Draft
Volume I of IV
(Do Not
Cite or Quote)
NOTICE
This document it a preliminary draft, it ha» not been formally
reieaaed by EPA and should not at this stag* be construed to
represent Agency policy. It is being circulated for comment on its
technical accuracy and policy implications.
-------
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DOCUMENT REVIEW FORM
Title/Draft
Air Quality Criteria for Lead
(External Review Draft #1)
ieturn to:
Project Officer for Lead
Environmental Criteria and
Assessment Office, U.S. EPA
MD-52
Research Triangle Park, NC 27711
Conmenter/Organisation/Addrest *
Chapter No./Title
RECOMMENDATIONS
P (1) Acceptable a* it
Additional Contributors to Document
Review (Hame and Affiliation)
0 (2) Acceptable after mimf revision
O (3) Aeceptable altar major revision
0 (4) Noi acceptable
W you have cheeked either 3 or 4,
pleise specifically state reaton(s) in
the comminH space 1m low.
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information.
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Draft
Do Not Quote or Cite
EPA-600/8-83-028A
October 1983
External Review Draft
Air Quality Criteria
for Lead
Volume I
NOTICE
This document is a preliminary draft. It has not bean formally released by EPA and should not at this stage
be construed to represent Agency policy. It is being circulated tor comment on its technical accuracy and
policy implications.
Environmental Criteria and Assessment Office
Office oif Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
-------
NOTICE
Mention of trade names or commercial products does not constitute
endorsement or recommendation for use.
11
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ABSTRACT
The document evaluates and assesses scientific information on the health
and welfare effects associated with exposure to various concentrations of lead
in ambient air. The literature through 1983 has been reviewed thoroughly for
information relevant to air quality criteria, although the document 1s not
intended as a complete and detailed review of all literature pertaining to
lead. An attempt has been made to identify the major discrepancies in our
current knowledge and understanding of the effects of these pollutants.
Although this document is principally concerned with the health and
welfare effects of lead, other scientific data are presented and evaluated 1n
order to provide a better understanding of this pollutant in the environment.
To this end, the document includes chapters that discuss the chemistry and
physics of the pollutant; analytical techniques; sources, and types of
emissions; environmental concentrations and exposure levels; atmospheric
chemistry and dispersion modeling; effects on vegetation; and respiratory,
physiological, toxicological, clinical, and epidemiological aspects of human
exposure.
ill
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PRELIMINARY DRAFT
CONTENTS
VOLUME I
Chapter 1. Executive Summary and Conclusions 1-1
VOLUME II
Chapter 2. Introduction 2-1
Chapter 3. Chemical and Physical Properties 3-1
Chapter 4. Sampling and Analytical Methods for Environmental Lead 4-1
Chapter 5. Sources and Emissions 5-1
Chapter 6. Transport and Transformation 6-1
Chapter 7. Environmental Concentrations and Potential Pathways to Human Exposure .. 7-1
Chapter 8. Effects of Lead on Ecosystems 8-1
VOLUME III
Chapter 9. Quantitative Evaluation of Lead and Biochemical Indices of Lead
Exposure in Physiological Media 9-1
Chapter 10. Metabolism of Lead 10-1
Chapter 11. Assessment of Lead Exposures and Absorption 1n Human Populations 11-1
Volume IV
Chapter 12. Biological Effects of Lead Exposure 12-1
Chapter 13. Evaluation of Human Health Risk Associated with Exposure to Lead
and Its Compounds 13-1
iv
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PRELIMINARY DRAFT
TABLE OF CONTENTS
CHAPTER'1
EXECUTIVE SUMMARY AND CONCLUSIONS
Page
LIST OF FIGURES v
LIST OF TABLES vi
1. EXECUTIVE SUMMARY AND CONCLUSIONS 1-1
1.1 INTRODUCTION 1-1
1.2 ORGANIZATION OF DOCUMENT 1-3
1.3 CHEMICAL AND PHYSICAL PROPERTIES OF LEAD 1-4
1.4 SAMPLING AND ANALYTICAL METHODS FOR ENVIRONMENTAL LEAD 1-6
1.4.1 Sampling Techniques 1-7
1.4.2 Analytical Procedures 1-10
1.5 SOURCES AND EMISSIONS 1-13
1.6 TRANSPORT AND TRANSFORMATION 1-22
1.7 ENVIRONMENTAL CONCENTRATIONS AND POTENTIAL PATHWAYS
TO HUMAN EXPOSURE 1-34
1.7.1 Lead in Air 1-34
1.7.2 Lead in Soil and Dust 1-37
1.7.3 Lead in Food 1-38
1.7.4 Lead in Water 1-39
1.7.5 Baseline Exposures to Lead 1-40
1.7.6 Additional Exposures 1-45
Urban atmospheres 1-45
Houses with interior lead paint 1-47
Family gardens 1-47
Houses with lead plumbing 1-47
Residences near smelters and refineries 1-48
Occupational exposures 1-48
Secondary occupational exposure 1-49
Special habits or activities 1-49
1.8 EFFECTS OF LEAD ON ECOSYSTEMS 1-52
1.8.1 Effects on Plants 1-57
1.8.2 Effects of Animals 1-61
1.8.3 Effects on Microorganisms 1-63
1.8.4 Effects on Ecosystems 1-64
1.8.5 Summary 1-66
1.9 QUANTITATIVE EVALUATION OF LEAO AND BIOCHEMICAL INDICES OF LEAD
EXPOSURE IN PHYSIOLOGICAL MEDIA 1-67
1.9.1 Determinations of Lead in Biological Media 1-67
Measurements of lead in blood 1-68
Lead in plasma 1-69
Lead in teeth 1-69 '
Lead in hair 1-69
Lead in urine 1-70
Lead 1 n other ti ssues 1-70
Quality assurance procedures in lead analyses 1-70
1.9.2 Determination of Erythrocyte Porphyrin (Free Erythrocyte
Protoporphyrin, Zinc Protoporphyrin) 1-71
1.9.3 Measurement of Urinary Coproporphyrin 1-72
CHP1D/B
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
Page
1.9.4 Measurement of Oelta-Aainolevulinic Acid Dehydrase Activity 1-72
1.9.5 Measurement of Delta-Aminolevulinic Acid in Urine and
Other Media 1-73
1.9.6 Measurement of Pyrimidine-51-Nucleotidase Activity 1-74
1.10 METABOLISM OF LEAD 1-74
1.10.1 Lead Absorption in Humans and Animals 1-75
Respiratory absorption of lead 1-75
Gastrointestinal absorption of lead 1-75
Percutaneous absorption of lead 1-76
Transplacental transfer of lead .. 1-76
1.10.2 Distribution of Lead in Humans and Animals 1-77
1.10.2.1 Lead in Blood 1-77
1.10.2.2 Lead Levels in Tissues 1-77
Soft tissues 1-78
Mineralizing tissue 1-78
Chelatable lead 1-79
Animal studies 1-79
1.10.3 Lead Excretion and Retention in Humans and Animals 1-80
Human studies 1-80
Animal studies 1-81
1.10.4 Interactions of Lead with Essential Metals and Other Factors ........ 1-81
Human studies 1-81
Animal studies 1-82
1.10.5 Interrelationships of Lead Exposure with Exposure Indicators
and Tissue Lead Burdens 1-82
Temporal characters!tics of Internal Indicators
of 1 ead exposure 1-83
Biological aspects of external exposure-
internal indicator relationships 1-83
Internal indicator-tissue lead relationships 1-83
1.10.6 Metabolism of Lead Alkyls 1-84
Absorption of lead alkyls in humans and animals 1-84
Biotransformation and tissue distribution of lead alkyls 1-85
Excretion of lead alkyls 1-85
1.11 ASSESSMENT OF LEAD EXPOSURES AND ABSORPTION IN HUMAN POPULATIONS 1-85
1.11.1 Levels of Lead and Demographic Covariates
in U.S. Populations 1-86
1.11.2 Blood Lead vs. Inhaled Air Lead Relationships 1-92
1.11.3 Dietary Lead Exposures Including Water 1-96
1.11.4 Studies Relating Lead in Soil and Dust to Blood Lead 1-97
1.11.5 Paint Lead Exposures 1-98
1.11.6 Specific Source Studies 1-99
1.11.7 Primary Smelters Populations .... ........ 1-102
1.11.8 Secondary Exposure of Children 1-105
1.12 BIOLOGICAL EFFECTS OF LEAD EXPOSURE 1-106
1.12.1 Introduction 1-106
1.12.2 Subcellular Effects of Lead 1-10#
1.12.3 Effects of Lead on Heme Biosynthesis, Erythropoiesis, and
Erythrocyte Physiology in Humans and Animals l-10f
1.12.4 Neurotoxic Effects of Lead 1-11$
1.12.5 Effects of Lead on the Kidney 1-111
vi
CHP1D/B 9/30/83
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
Page
1.12.6 Effects of Lead on Reproduction and Development 1-121
1.12.7 Genotoxic and Carcinogenic Effects of Lead 1-122
1.12.8 Effects of Lead on the Imune Systen 1-123
1.12.9 Effects of Lead on Other Organ Systens 1-123
1.13 EVALUATION OF HUNAN HEALTH RISKS ASSOCIATED WITH EXPOSURE TO LEAD ANO
ITS COMPOUNDS 1-123
1.13.1 Introduction 1-123
1.13.2 Exposure Aspects 1-124
1.13.3 Lead Metabolism: Key Issues for Hunan Health Risk Evaluation 1-130
1.13.4 Biological Effects of Lead Relevant to the General Human Population . 1-136
1.13.5 Dose-Response Relationships for Lead Effects in Human Populations ... 1-145
1.13.6 Populations at Risk 1-148
1.13.7 Summary and Conclusions 1-151
vi1
CHP1D/B 9/30/83
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PRELIMINARY DRAFT
LIST OF TABLES
Table Page
1-1 Estimated ataiospheric lead emissions for the United States, 1981 and
the world 1-17
1-2 Summary of surrogate and vegetation surface deposition of lead 1-30
1-3 Estimated global deposition of atmospheric lead 1-31
1-4 Atmospheric lead in urban, rural, and remote areas of the world 1-35
1-5 Background lead in basic food crops and meats 1-39
1-6 Summary of environmental concentrations of lead 1-41
1-7 Summary by age and sex of estimated average levels of lead ingested
from mi 1 k and foods 1-43
1-8 Summary of baseline human exposures to lead 1-46
1-9 Weighted geometric mean blood lead levels from NHANES II survey by
degree of urbanization of place of residence in the U.S. by age
and race, United States 1976-80 1-89
1-10 Summary of pooled geometric standard deviations and estimated
analytic errors 1-93
1-11 Summary of blood inhalation slopes yg/dl per pg/m? 1-94
1-12 Estimated contribution of leaded gasoline to blood lead by inhalation
and non-inhalation pathways 1-101
1-13 Summary of baseline human exposures to lead 1-126
1-14 Relative baseli human lead exposures expressed per kilogram body weight 1-127
1-15 Summary of potential additive exposures to lead 1-128
1-16 Direct contributions of air lead to blood lead (Pb8) in adults at fixed
inputs of water and food lead 1-135
1-17 Direct contributions of air >ead to blood lead in children at fixed inputs
of water and food lead 1-135
1-18 Contributions of dust/soil lead to blood lead in children at fixed inputs
of a1 r, food, and water lead 1-135
1-19 Summary of lowest observed effect levels for key lead-induced health effects
in adults 1-139
1-20 Summary of lowest observed effect levels for key lead-induced health effects
in children 1-141
1-21 EPA-estimated percentage of subjects with ala-u exceeding limits for
various blood lead levels 1-147
1-22 Provisional estimate of the number of individuals in urban and rural
population segments at greatest potential risk to lead exposure 1-151
CHP1D/B
viii
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PRELIMINARY DRAFT
LIST OF FIGURES
Figure Page
1-1 Pathways of lead exposure from the environment to nan 1-2
1-2 Metal complexes of lead 1-5
1-3 Softness parameters of metals , 1-6
1-4 Chronological record of the relative increase of lead in snow strata,
pond and lake sediments, marine sediments, and tree rings. The data
are expressed as a ratio of the latest year of the record and should
not be interpreted to extend back in time to natural or uncontaminated
levels of lead concentration 1-14
1-5 The global lead production has changed historically in response to
major economic and political events. Increases in lead production
(note log scale) correspond approximately to historical increases
in lead emissions shown in Figure 1-4 1-15
1-6 Locations of major lead operations in the United States 1-18
1-7 Trend 1n lead content of U.S. gasolines, 1975-1982 1-20
1-8 Relationship between lead consumed in gasoline and composite
maximum quarterly average lead levels, 1975-1980 1-21
1-9 Profile of lead concentrations in the central northeast Pacific. Values
below 1000 m are an order magnitude lower than reported by Tatsumoto and
Patterson (1963) and Chow and Patterson (1966) 1-26
1-10 Lead concentration profile in snow strata of northern Greenland 1-27
1-11 Variation of lead saturation capacity with cation exchange capacity in
soil at selected pH values 1-32
1-12 This figure depicts cycling process within major components of a terrestrial
ecosystem, i.e. primary producers, grazers, and decomposers. Nutrient and
non-nutrient elements are stored in reservoirs within these components.
Processes that take place within reservoirs regulate the flow of elements
between reservoirs along established pathways. The rate of flow is in
part a function of the concentration in the preceding reservoir. Lead
accumulates in decomposer reservoirs which have a high binding capacity
for this metal. It is likely that the rate of flow away from these
reservoirs has increased in past decades and will continue to increase
for some time until the decomposer reservoirs are in equilibrium with the
entire ecosystem. Inputs to and outputs from the ecosystems as a whole
are not shown 1-54
1-13 Geometric mean blood lead levels by race and age for younger children in the
NHANES II study, and the Kellogg/Silver Valley and New York childhood
screening studies 1-87
1-14 Average blood lead levels of U.S. population 6 months - 74 years. United
States, February 1976 - February 1980, based on dates of examination of
NHANES II examinees with blood lead determinations 1-90
1-15 Time dependence of blood lead for blacks, aged 24 to 35 months, in New York
City and Chicago 1-91
1-16 Change in 20*Pb/®W7Pb ratios in petrol, airborne particulate and
blood from 1974 to 1981 1-100
1-17 Geometric mean blood lead levels of New York City children (aged 25-36
months) by ethnic group, and ambient air lead concentration vs.
quarterly sampling period, 1970-1976 1-103
1-18 Geometric mean blood lead levels of New York City children (aged 25-36
months) by ethnic group, and estimated amount of lead present in gasoline
sold in New York, New Jersey, and Connecticut vs. quarterly sampling
period, 1970-1976 1-104
ix
CHP1D/8 9/30/83
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PRELIMINARY DRAFT
LIST OF FIGURES (continued).
Figure Page
1-19 Dose-response for elevation of EP as a function of blood lead level using
probit analysis 1-146
1-20 Dose-response curve for FEP as a function of blood lead level: in sub-
populations ..... 1-146
1-21 EPA calculated dose-response for ALA-lt 1-147
CHP1D/B
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AUTHORS AND CONTRIBUTORS
Chapter 1: Executive Sumary
Principal Author
Dr. Lester D. Grant
Director
Environmental Criteria and Assessment
Environmental Protection Agency
MD-52
Research Triangle Park, NC 27711
Contributing Authors:
Dr. J. Michael Davis
Environmental Criteria and
Assessment Office
MD-52
Research Triangle Park, NC 27711
Dr. Vic Hasselblad
Biometry Division
Health Effects Research Laboratory
MD-55
Research Triangle Park, NC 27711
Dr. Paul Mushak
Department of Pathology
School of Medicine
University of North Carolina
Chapel Hill, NC 27514
Dr. Robert W. Elias
Environmental Criteria and
Assessment Office
MD-52
Research Triangle Park, NC 27711
Dr. Dennis J. Kotchmar
Environmental Criteria and
Assessment Office
MD-52
Research Triangle Park, NC 27711
Dr. David E. Weil
Environmental Criteria and
and Assessment Office
MD-52
Research Triangle Park, NC 27711
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS
AAS
Ach
ACTH
AOCC
ADP/O ratio
AIDS
AIHA
All
ALA
ALA-D
ALA-S
ALA-U
APDC
APHA
ASTM
ASV
ATP
B-cells
Ba
BAL
BAP
BSA
BUN
BW
C.V.
CaBP
CaEDTA
CBD
Cd
CDC
CEC
CEH
CFfi
CMP
CNS
CO
COHb
CP-U
cBah
D.F,
DA
DCMU
DDP
DNA
DTH
EEC
EEG
EMC
EP
EPA
Atomic absorption spectrometry
Acetylcholine
Adrenocoticotrophic hormone
Antibody-dependent cell-mediated cytotoxicity
Adenosine diphosphate/oxygen ratio
Acquired Immune deficiency syndrome
American Industrial Hygiene Association
Angiotensin II
Aminolevulinic acid
Aminolevulinic acid dehydrase
Aminolevulinic acid synthetase
Aminolevulinic acid in urine
Ammonium pyrrolidine-dlthiocarbamate
American Public Health Association
Amerclan Society for Testing and Materials
Anodic stripping voltammetry
Adenosine triphosphate
Bone marrow-derived lymphocytes
Barium
British anti-Lewisite (AKA dimercaprol)
ben20(a)pyrene
Bovine serum albumin
Blood urea nitrogen
Body weight
Coefficient of variation
Calcium binding protein
Calcium ethylenediaminetetraacetate
Central business district
Cadmium
Centers for Disease Control
Cation exchange capacity
Center for Environmental Health
reference method
Cytidine monophosphate
Central nervous system
Carbon monoxide
Carboxyhemoglobin
Urinary coproporphyrin
plasma clearance of p-aminohippuric acid
Copper
Degrees of freedom
Dopamine
£3-(3,4-dlchloropheny1)-1,l-dimethylurea
Differential pulse polarography
Deoxyribonucleic acid
Delayed-type hypersensitivity
European Economic Community
Electroencephalogram
Encephalomyocarditis
Erythrocyte protoporphyrin
U.S. Environmental Protection Agency
TCPBA/D Xtt 9/20/83
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
FA Fulvie add
FDA Food and Drug Administration
Fe Iron
FEP Free erythrocyte protoporphyrin
FY Fiscal year
G.N. Grand nean
G-6-PD Glucose-6-phosphate dehydrogenase
GABA Gamma-aminobutyr1c acid
GALT Gut-associated lymphoid tissue
GC Gas chromatography
GFR Glomerular filtration rate
HA Humic acid
Hg Mercury
hi-vol High-volume air sampler
HPLC High-performance liquid chromatography
i.m. Intramuscular (method of injection)
i.p. Intraperitoneal1y (method of injection)
i.v. Intravenously (method of injection)
IAA Indol-3-ylacetic acid
IARC International Agency for Research on Cancer
ICD International classification of diseases
ICP Inductively coupled plasma
IDHS Isotope dilution mass spectrometry
IF Interferon
ILE Isotopic Lead Experiment (Italy)
IRPC International Radiological Protection Commission
K Potassium
LAI Leaf area index
LDH-X Lactate dehydrogenase isoenzyme x
LC,.- Lethyl concentration (50 percent)
ID,- Lethal dose (50 percent)
LH Luteinizing hormone
LIP0 Laboratory Improvement Program Office
In National logarithm
LPS Lipopolysaccharide
LRT Long range transport
mRNA Messenger ribonucleic acid
ME Mercaptoethanol
MEPP Miniature end-plate potential
MES Maximal electroshock seizure
MeV Mega-electron volts
MLC Mixed lymphocyte culture
MMD Mass median diameter
MMED Mass median equivalent diameter
Mn Manganese
MND Motor neuron disease
MSV Moloney sarcoma virus
MTO Maximum tolerated dose
n Number of subjects
N/A Not Available
xiii
TCPBA/D 9/20/83
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS
NA Not Applicable
NAAQS National ambient air quality standards
NADB National Aerometric Oata Bank
NAHS National A1r Monitoring Station
NAS National Academy of Sciences
NASN National Air Surveillance Network
NBS National Bureau of Standards
NE Norepinephrine
NFAN National Filter Analysis Network
NFR-82 Nutrition Foundation Report of 1982
NHANES II National Health Assessment and Nutritional Evaluation Survey II
Ni Nickel
OSHA Occupational Safety and Health Administration
P Potassium
p Significance symbol
PAH Para-aminohippuric acid
Pb Lead
PBA Air lead
Pb(Ac), Lead acetate
PbB concentration of lead 1n blood
PbBrCl Lead (II) bromochloride
PBG Porptiob111nogen
PFC Plaque-forming cells
pH Measure of acidity
PHA Phytohemagglutinin
PHZ Polyacry1amide-hydrous-zi rconi a
PIXE Proton-induced X-ray emissions
PMN Polymorphonuclear leukocytes
PND Post-natal day
PNS Peripheral nervous system
ppm Parts per million
PRA Plasma renin activity
PRS Plasma renin substrate
PWM Pokeweed mitogen
Py-5-N Pyrimlde-5'-nucleotidase
RBC Red blood cell; erythrocyte
RBF Renal blood flow
RCR Respiratory control ratios/rates
redox Oxidation-reduction potential
RES Reticuloendothelial system
RLV Rauscher leukemia virus
RNA Ribonucleic acid
S-HT Serotonin
SA-7 Simian adenovirus
scm Standard cubic meter
S.D. Standard deviation
SDS Sodium dodecyl sulfate
S.E.M. Standard error of the mean
SES Socioeconomic status
SCOT Serum glutamic oxaloacetic transaminase
x1v
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
slg
SLAMS
SMR
Sr
SRBC
SRMs
STEL
SW voltage
T-cel1s
t-tests
TBL
TEA
TEL
TIBC
TML
TMLC
TSH
TSP
U.K.
UMP
USPHS
VA
Sfe
WHO
KRF
In
ZPP
Surface immunoglobulin
State and local air monitoring stations
Standardized mortality ratio
Strontlurn
Sheep red blood cells
Standard reference Materials
Short-tern exposure limit
Slow-wave voltage
Thymus-derlved lymphocytes
Tests of significance
Trl-n-butyl lead
Tetraethyl-ammonium
Tetraethyllead
Total iron binding capacity
Tetrame thy Head
Tetramethyl1ead chloride
Thyroid-stimulating hormone
Total suspended particulate
United Kingdom
Uridine monophosphate
U.S. Public Health Service
Veterans Administration
Deposition velocity
Visual evoked response
World Health Organization
X-Ray fluorescence
Chi squared
Zinc
Erythrocyte zinc protoporphyrin
MEASUREMENT ABBREVIATIONS
dl
ft
g
g/gal
g/ha-mo
km/hr
1/mln
mg/km
jig/ms
RMI
MHiol
ng/cm2
not
nM
sec
deciliter
feet
gram
gram/gallon
gran/hectare•month
kilometer/hour
liter/minute
milligram/kilometer
microgram/cubic meter
millimeter
micrometer
nanograms/square centimeter
namometer
nanomole
second
xv
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PRELIMINARY DRAFT
1. EXECUTIVE SUMMARY AND CONCLUSIONS
1.1 INTRODUCTION
This criteria document evaluates and assesses scientific information on the health and
welfare effects associated with exposure to various concentrations of lead in ambient air.
According to Section 108 of the Clean Air Act of 1970, as amended in June 1974, a cri-
teria document for a specific pollutant or class of pollutants shall:
. . . accurately reflect the latest scientific knowledge useful in indicating
the kind and extent of all identifiable effects on public health or welfare which
¦ay be expected from the presence of such pollutant in the ambient air, in varying
quantities.
Air quality criteria are of necessity based on presently available scientific data, which
in turn reflect the sophistication of the technology used in obtaining those data as well as
the magnitude of the experimental efforts expended. Thus air quality criteria for atmospheric
pollutants are a scientific expression of current knowledge and uncertainties. Specifically
air quality criteria are expressions of the scientific knowledge of the relationships between
various concentrations—averaged over a suitable time period—of pollutants in the same atmos-
phere and their adverse effects upon public health and the environment. Criteria are issued
as a basis for making decisions about the need for control of a pollutant and as a basis for
development of air quality standards governing the pollutant. Air quality criteria are
descriptive; that is, they describe the effects that have been observed to occur as a result
of external exposure at specific levels of a pollutant. In contrast, air quality standards
are prescriptive; that is, they prescribe what a political jurisdiction has determined to be
the Maximum permissible exposure for a given time in a specified geographic area.
This criteria document 1s a revision of the previous Air Quality Criteria Document for
Lead (EPA-600/8-77-017) published in December, 1977. This revision is mandated by the Clean.
Air Act (Sect. 108 and 109), as amended UXS.C. §§7408 and 7409. The criteria document sets
forth what is known about the effects of lead contamination in the environment on human health
and welfare. This requires that the relationship between levels of exposure to lead, via all
routes and averaged over a suitable time period, and the biological responses to those levels
be carefully assessed. Assessment of exposure must take into consideration the temporal and
spatial distribution of lead and its various forms in the environment. Thus, the literature
through June, 1983, has been reviewed thoroughly for information relevant to air quality cri-
teria, for lead, but the document is not intended as a complete and detailed review of all
literature pertaining to lead. Also, efforts are made to identify major discrepancies in "our
current knowledge and understanding of the effects of lead compounds.
SUHPB/D
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9/30/83
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PRELIMINARY DRAFT
Lead is a naturally occurring element that nay be found in the earth's crust and in all
components of the biosphere. It nay be found 1n water, soil, plants, animals, and humans.
Because lead also occurs in ore bodies that have been mined for centuries by man, this metal
has also been distributed throughout the biosphere by the industrial activities of man. Of
particular Importance to the human environment are emissions of lead to'the atmosphere. The
sources of these emissions and the pathways of lead through the environment to man are shown
in Figure 1-1. This figure shows natural inputs to soil by crustal weathering and
anthropogenic inputs to the atmosphere from automobile emissions and stationary industrial
sources. Natural emissions of lead to the atmosphere from volcanoes and windblown soil are of
minor importance.
AUTO
EMISSIONS
CRUSTAL
WEATHERING
AMBIENT
AIR
SURFACE AND
GROUND WATER
SOIL
PLANTS
ANIMALS
INHALED
AIR
DRINKING
WATER
DUSTS
FOOD
MAN
SOFT
TI88UE
BLOOD
tf
BONES
UVERf
KIDNEY
FECES URINE
SUMPB/0
Fi^ira 1-1. Pithwayi of tmtl exposure from the environment to men.
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From these emission sources, lead moves through the atmosphere to various components of
the human environment. Lead is deposited on soil and plants and in animals, becoming incor-
porated into the food chain of man. Atmospheric lead is a major component of household and
street dust; lead is also inhaled directly from the atmosphere.
1.2 ORGANIZATION OF DOCUMENT
This document focuses primarily on lead as found in its various forms in the ambient
atmosphere; in order to assess its effects on human health, however, the distribution and bio*
logical availability of lead in other environmental media have been considered. The rationale
for structuring the document was based primarily on the two major questions of exposure and
response. The first portion of the do'cument 1s devoted to lead in the environment—its physi-
cal and chemical properties; the monitoring of lead in various media; sources, emissions, and
concentrations of lead; and the transport and transformation of lead within environmental
media. The latter portion is devoted to biological responses and effects on human health and
ecosystems.
In order to facilitate printing, distribution, and review of the present draft materials,
this First External Review Draft of the revised EPA Air Quality Criteria Document for Lead is
being released in four volumes. The first volume (Volume I) contains this executive summary
and conclusions chapter (Chapter 1) for the entire document. Volume II contains Chapters 2-8,
which include: the introduction for the document (Chapter 2); discussions of the above listed
topics concerning lead in the environment (Chapters 3-7); and evaluation of lead effects on
ecosystems (Chapter 8). The remaining two volumes contain Chapters 9-13, which deal with the
extensive available literature relevant to assessment of health effects associated with lead
exposure.
An effort has been made to limit the document to a highly critical assessment of the sci-
entific data base. The scientific literature has been reviewed through June 1983. The refer-
ences cited do not constitute an exhaustive bibliography of all available lead-related litera-
ture but they are thought to be sufficient to reflect the current state of knowledge on those
issues most relevant to the review of the air quality standard for lead.
The status of control technology for lead is not discussed in this document. For informa-
tion on the subject, the reader 1s referred to appropriate control technology documentation
published by the Office of A1r Quality Planning and Standards (OAQPS), EPA. The subject of
"adequate margin of safety" stipulated 1n Section 108 of the Clean Air Act also is not expli-
citly addressed here; this topic will be considered in depth by EPA's Office of A1r Quality
Planning and Standards in documentation prepared as a part of the process of revising the Na-
tional Ambient Air Quality Standard (NAAQS) for Lead.
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1.3 CHEMICAL AND PHYSICAL PROPERTIES OF LEAD
Lead is a gray-white metal of bright luster that, because of its easy isolation and low
¦elting point, was aiwng the first of the metals to be extensively utilized by nan. Lead was
used as early as 2000 B.C. by the Phoenicians. The most abundant ore is galena, from which
metallic lead is readily smelted. The metal is soft, malleable, and ductile, a poor
electrical conductor, and highly impervious to corrosion. This unique combination of physical
properties has led to its use in piping and roofing, and 1n containers for corrosive liquids.
The metal and the dioxide are used in storage batteries, and organolead compounds are used in
gasoline additives to boost octane levels. Since lead occurs in highly concentrated ores from
which it is readily separated, the availability of lead is far greater than its natural abun-
dance would suggest. The great environmental significance of lead is the result both of its
utility and of its availability.
The properties of organolead compounds (i.e., compounds containing bonds between lead and
carbon) are entirely different from those of the inorganic compounds of lead. Because of their
use as antiknock agents in gasoline and other fuels, the most important organolead compounds
have been the tetraalkyl compounds tetraethyllead (TEL) and tetramethyllead (TML). These lead
compounds are removed from internal combustion engines by a process called lead scavenging, in
which they react in the combustion chamber with halogenated hydrocarbon additives (notably
ethylene dibronide and ethylene dichloride) to form lead halides, usually bronochlorolead(II).
The donor atoms in a metal complex could be almost any basic atom or molecule; the gnly
requirement is that a donor, usually called a ligand, must have a pair of electrons available
for bond formation. In general, the metal atom occupies a central position in the complex, as
exemplified by the lead atom in tetramethyllead (Figure l-2a) which is tetrahedrally sur-
rounded by four methyl groups. In these simple organolead compounds, the lead is usually pre-
sent as Pb(IV), and the complexes are relatively inert. These simple ligands, which bind to
metal at only a single site, are called monodentate ligands. Some Ugands, however, can bind
to the metal atom by more than one donor atom, so as to form a heterocyclic ring structure.
Rings of this general type are called chelate rings, and the donor molecules which form them
are called polydentate ligands or chelating agents. In the chemistry of lead, chelation nor-
mally involves Pb(II). A wide variety of biologically significant chelates with ligands
such as amino acids, peptides, and nucleotides are known. The simplest structure of this
type occurs with the amino acid glycine, as represented in Figure l-2b for a 1:2
(metal;ligand) complex. The importance of chelating agents in the present context is their
widespread use in the treatment of lead and other metal poisoning.
SUMPB/D
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H2O
h3c CH3 V/\ !
\/ f \:X CV2
Pb Pb
/ \ CH2x /'\
Hac CH3 NH2 1 xo^
H20
(a) (b)
Figure 1-2. Metal complexes of lead.
Metals are often classified according to some combination of their electronegativity,
Ionic radius, and formal charge. These parameters are used to construct empirical classifi-
cation schemes of relative hardness or softness. In these schemes, "hard" metals form strong
bonds with "hard" anions and, likewise, "soft" metals bond with "soft" anions. Some metals
are borderline, having both soft and hard character. Pb(II), although borderline, demon-
strates primarily soft character (Figure 1-3). The term Class A may also be used to refer to
hard metals, and Class B to soft metals. Since Pb(II) is a relatively soft (or class B) metal
ion, it forms strong bonds to soft donor atoms like the sulfur atoms in the cysteine residues
of proteins and enzymes. In living systems, lead atoms bind to these peptide residues in pro-
teins, thereby changing the tertiary structure of the protein or blocking a substrate's
approach to the active site of an enzyme. This prevents the proteins from carrying out their
functions. As has been demonstrated in several studies (Jones and Vaughn, 1978; Williams and
Turner, 1981; Williams et al., 1982), there is an inverse correlation between the LD^ values
of metal complexes and the chemical softness parameter. Lead(II) has a higher softness para-
meter than either cadmium(II) or mercury(II), so lead(II) compounds would not be expected to
be as toxic as their cadmium or mercury analogues.
The role of the chelating agents is to compete with the peptides for the metal by forming
stable chelate complexes that can be transported from the protein and eventually be excreted
by the body. For simple thermodynamic reasons, chelate complexes are much more stable than
monodentate metal complexes, and it is this enhanced stability that is the basis for their
ability to compete favorably with proteins and other Hgands for the metal ions.
SUNPB/D
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• i—T
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o
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• Bl"
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CLASS A OR IONIC INDEX, Z'/r
Figure 1-3. Softness parameters of metals.
Source: Nieboer and Richardson (1980).
It should be noted that both the stoichiometry and structures of metal chelates depend
upon pH, and that structures different from those manifest in solution may occur in crystals.
It will suffice to state, however, that several Ugands can be found that are capable of suf-
ficiently strong chelation with lead present In the body under physiological conditions to
permit their use in the effective treatment of lead poisoning.
1.4 SAMPLING AND'ANALYTICAL METHODS FOR ENVIRONMENTAL LEAD
Lead-, like all criteria pollutants, has a designated Reference Method for monitoring and
analysis as required in State Implementation Plans for determining compliance with the lead
National Ambient Air Quality Standard. The Reference Method uses a high volume sampler (hi-
vol) for sample collection and atomic absorption spectrometry (AAS) for analysis.
For a rigorous quality assurance program, it is essential that investigators recognize
all sources of contamination and use every precaution to eliminate them. Contamination occurs
SUMPB/D
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on the surfaces of collection containers and devices, on the hands and clothing of the inves-
tigator, in the chemical reagents, in the laboratory atmosphere, and on the labware and tools
used to prepare the sample for analysis.
1.4.1 Sampling Techniques
Sampling strategy encompasses site selection, choice of instrument used to obtain repre-
sentative samples, and choice of method used to preserve sample integrity. In the United States,
some sampling stations for air pollutants have been operated since the early 1950's. These
early stations were a part of the National A1r Surveillance Network (NASN), which has now
become the National Filter Analysis Network (NFAN). Two other types of networks have been
established to meet specific data requirements. State and Local Air Monitoring Stations
(SLAMS) provide data from specific areas where pollutant concentrations and population densi-
ties are the greatest and where monitoring of compliance to standards is critical. The Na-
tional Air Monitoring Station (NAMS) network is designed to serve national monitoring needs,
including assessment of national ambient trends. SLAMS and NAMS stations are maintained by
state and local agencies and the air samples are analyzed in their laboratories. Stations in
the NFAN network are maintained by state and local agencies, but the samples are analyzed by
laboratories 1n the U.S. Environmental Protection Agency, where quality control procedures are
rigorously maintained.
Data from all three networks are combined into one data base, the National Aerotietric
Data Bank (NADB). These data may be individual chemical analyses of a 24-hour sampling period
arithmetically averaged over a calendar period, or chemical composites of several filters used
to determine a quarterly composite. Data are occasionally not available for a given location
because they do not conform to strict statistical requirements.
In September, 1981, EPA promulgated regulations establishing ambient air monitoring and
data reporting requirements for lead comparable to those already established in May of 1979
for the other criteria pollutants. Whereas sampling for lead is accomplished when -sampling
for total suspended particulate (TSP), the designs of lead and TSP monitoring stations must be
complimentary to insure compliance with the NAMS criteria for each pollutant.
There must be at least two SLAMS sites for lead in any area that has a population greater
than 500,000 and any area where lead concentration currently exceeds the ambient lead standard
(1.5 Mg/"3) or has exceeded it since January 1, 1974.
To clarify the relationship between monitoring objectives and the actual siting of a mon-
itor, the concept of a spatial scale of representativeness was developed. The spatial scales
are discribed in terms of the physical dimensions of the air space surrounding the monitor
throughout which pollutant concentrations are fairly similar.
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The time scale may also be an important factor. Siting criteria must include sampling
times sufficiently long to include average wlndspeed and direction, or a sufficient number of
samples must be collected over short sampling periods to provide an average value consistent
with a 24-hour exposure.
Airborne lead is primarily inorganic particulate matter but may occur in the form of or-
ganic gases. Devices used for collecting samples of ambient atmospheric lead include the
standard hi-vol sampler and a Variety of other collectors employing filters, Impactors,
impingegers, or scrubbers, either separately or in combination, that measure lead in pg/m3.
2
Some samplers measure lead deposition expressed in "» some instruments separate parti-
cles by size. As a general rule, particles smaller in aerodynamic diameter than 2.5 pm are
classified as "fine", and those larger than 2.5 pm as "coarse."
The present SLAMS and NAMS employ the standard hi-vol sampler (U.S. Environmental Protec-
tion Agency, 1971) as part of their sampling networks. As a Federal Reference Method Sampler,
the hi-vol operates with a specific flow rate of 1600 to 2500 m3 of air per day
When sampling ambient lead with systems employing filters, it is likely that vapor-phase
organolead compounds will pass through the filter media. The use of bubblers downstream from
the filter containing a suitable reagent or absorber for collection of these compounds has
been shown to be effective. Organolead may be collected on iodine crystals, adsorbed on acti-
vated charcoal, or absorbed in an iodine monochloride solution. In one experiment, Purdue et
al. (1973) operated two bubblers in series containing iodine monochloride solution. One hun-
dred percent of the lead was recovered in the first bubbler.
Sampling of stationary sources for lead requires the use of a sequence of samplers in the
smokestack. Since lead in stack emissions may be present in a variety of physical and chemical
forms, source sampling trains must be designed to trap and retain both gaseous and particulate
lead.
Three principal procedures have been used to obtain samples of auto exhaust aerosols for
subsequent analysis for lead compounds: a horizontal dilution tunnel, plastic sample collec-
tion bags, and a low residence time proportional sampler. In each procedure, samples are air
diluted to simulate roadside exposure conditions. In the most commonly used procedure, the
air dilution tube segregates fine combustion-derived particles from larger lead particles.
Such tunnels of varying lengths have been limited by exhaust temperatures to total flows above
approximately 11 ma/mtn. Similar tunnels have a centrifugal fan located upstream, rather than
a positive displacement pump located downstream. This geometry produces a slight positive
pressure in the tunnel and expedites transfer of the aerosol to holding chambers for studies
of aerosol growth. However, turbulence from the fan may affect the sampling efficiency.
Since the total exhaust plus dilution airflow is not held constant in this system, potential
errors can be reduced by maintaining a very high dilution air/exhaust flow ratio.
SUMPB/D 1-8 9/30/83
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In the bag technique, auto emissions produced during simulated driving cycles are air-
diluted and collected in a large plastic bag. The aerosol sample is passed through a filtra-
tion or impaction sampler prior to lead analysis. This technique may result in errors of
aerosol size analysis because of condensation of low vapor pressure organic substances onto
the lead particles.
To minimize condensation problems, a third technique, a low residence tine proportional
sampling system, has been used. It is based on proportional sampling of raw exhaust, again
diluted with ambient air followed by filtration or Impaction. Since the sample flow must be a
constant proportion of the total exhaust flow, this technique may be limited by the response
time of the equipment to operating cycle phases that cause relatively small transients in the
exhaust flow rate.
Other primary environmental media that may be affected by airborne lead include precipi-
tation, surface water, soil, vegetation, and foodstuffs. The sampling plans and the sampling
methodologies used 1n dealing with these media depend on the purpose of the experiments, the
types of measurements to be carried out, and the analytical technique to be used.
Lead at the start of a rain event 1s higher 1n concentration than at the end, and rain
striking the canopy of a forest may rinse dry deposition particles from the leaf surfaces.
Rain collection systems should be designed to collect precipitation on an event basis and to
collect sequential samples during the event.
Two automated systems have recently been used. The Sangamo Precipitation Collector,
Type A, collects rain in a single bucket exposed at the beginning of the rain event (Samant
and Vaidya, 1982). A second sampler, described by Coscio et al. (1982), also remains covered
between rain events; it can collect a sequence of eight samples during the period of rain and
may be fitted with a refrigeration unit for sample cooling.
Because the physicochemlcal form of lead often influences environmental effects, there is
a need to differentiate among the various chemical forms. Complete differentiation among all
such forms is a complex task that has not yet been fully accomplished. The most commonly used
approach is to distinguish between dissolved and suspended forms of lead. All lead passing
through a 0.45 m" membrane filter is operationally defined as dissolved, while that retained
on the filter Is defined as suspended (Kopp and McKee, 1979).
Containers used for sample collection and storage should be fabricated from essentially
lead-free plastic or glass, e.g., conventional polyethylene, Teflon®, or quartz. These con-
tainers must be leached with hot acid for several days to ensure minimum lead contamination
(Patterson and Settle, 1976).
The distance from emission sources and depth gradients associated with lead in soil must
be considered in designing the sampling plan. Vegetation, litter, and large objects such as
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stones should not be Included 1n the sample. Depth samples should be collected at not greater
than 2 cm intervals to preserve vertical integrity.
Because most soil lead is in chemical forms unavailable to plants, and because lead is
not easily transported by plants, roots typically contain very little lead and shoots even
less. Before analysis, a decision must be made as to whether or not the plant leaf material
should be washed to remove surface contamination from dry deposition and soil particles. If
the plants are sampled for total lead content (e.g., if they serve as animal food sources),
they cannot be washed; if the effect of lead on internal plant processes is being studied, the
plant samples should be washed. In either case, the decision must be made at the time of sam-
pling, as washing cannot be effective after the plant materials have dried.
In sampling for airborne lead, air is drawn through filter materials such as glass fiber,
cellulose acetate, or porous plastic. These materials often include contaminant lead that can
Interfere with the subsequent analysis. Procedures for cleaning filters to reduce the lead
blank rely on washing with acids or complexing agents. The type of filter and the analytical
method to be used often determines the ashing technique. In some methods, e.g., X-ray fluo-
rescence, analysis can be performed directly on the filter if the filter material is suitable.
Skogerboe (1974) provided a general review of filter materials.
The main advantages of glass fiber filters are low pressure drop and high particle col-
lection efficiency at high flow rates. The main disadvantage is variability 1n the lead blank,
which makes their use inadvisable in many cases. This has placed a high priority on the stan-
dardization of a suitable filter for hi-vol samples. Other investigations have indicated,
however, that glass fiber filters are now available that do not present a lead interference
A
problem (Scott et al., 1976b). Teflon filters have been used since 1975 by Dzubay et al.
(1982) and Stevens et al. (1978), who have shown these filters to have very low lead blanks
(<2 ng/cm2). The collection efficiencies of filters, and also of impactors, have been shown
to be dominant factors in the quality of the derived data.
1.4.2 Analytical Procedures
The choice of analytical method depends on the nature of the data required, the type of
sample being analyzed, the skill of the analyst, and the equipment available. For general
determination of elemental lead, atomic absorption spectroscopy (AAS) 1s widely used and re-
commended (C.F.R., 1982 40: § 50). Optical emission spectrometry and X-ray fluorescence
(XRF) are rapid and inexpensive methods for multlelemental analyses. X-ray fluorescence can
measure lead concentrations reliably to 1 ng/m3 using samples collected with commercial
dichotomous samplers. Other analytical methods have specific advantages appropriate for
special studies.
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With respect to measuring lead without contamination during sampling or from the labora-
tory, several Investigators have shown that the magnitude of the problem Is quite large. It
appears that the problem may be caused by failure to control the blank or by failure to stan-
dardize instrument operation (Patterson, 1983; Skogerboe, 1982). The laboratory atmosphere,
collecting containers, and the labware used may be primary contributors to the lead blank
problem (Patterson, 1983; Skogerboe, 1982). Failure to recognize these and other sources of
contamination such as reagents and hand contact 1s very likely to result 1n the generation of
artificially high analytical results. Samples with less than 100 ng lead should be analyzed
in a clean laboratory especially designed for the elimination of lead contamination. Moody
(1982) has described the construction and application of such a laboratory at the National
Bureau of Standards.
For AAS, the lead atoms in the sample must be vaporized either 1n a precisely controlled
flame or In a furnace. Furnace systems in AAS offer high sensitivity as well as the ability
to analyze small samples. These enhanced capabilities are offset in part by greater dif-
ficulty In analytical calibration and by loss of analytical precision.
Particles may also be collected on cellulose acetate filters. Disks (0.5 cm2) are
punched from these filters and analyzed by insertion of nlchrome cups containing the disks
into a flame. Another application Involves the use of graphite cups as particle filters with
the subsequent analysis of the cups directly in the furnace system. These two procedures
offer the ability to determine particulate lead directly with minimal sample handling.
In an analysis using AAS and hi-vol samplers, atmospheric concentrations of lead were
found to be 0.076 ng/m3 at the South Pole (Maenhaut et al., 1979). Lead analyses of 995 par-
ticulate samples from the NASN were accomplished by AAS with an indicated precision of 11 per-
cent (Scott et al., 1976a). More specialized AAS methods for the determination of tetraalkyl
lead compounds in water and fish tissue have been described by Chau et al. (1979) and in air
by B1rn1e and Noden (1980) and Rohbock et al. (1980).
Techniques for AAS are still evolving. An alternative to the graphite furnace, evaluated
by J1n and Taga (1982), uses a heated quartz tube through which the metal 1on in gaseous
hydride form flows continuously. Sensitivities were 1 to 3 ng/g for lead. The technique 1s
similar to the hydride generators used for mercury, arsenic, and selenium. Other nonflame
atomlzatlon systems, electrodeless discharge lamps, and other equipment refinements and tech-
nique developments have been reported (Horllck, 1982).
Optical emission spectroscopy 1s based on the measurement of the light emitted by
elements when they are excited In an appropriate energy medium. The technique has been used
to determine the lead content of soils, rocks, and minerals at the 5 to 10 nfl/fl level with a
relative standard deviation of 5 to 10 percent; this method has also been applied to the ana-
lysis of a large number of air samples (Sugimae and Skogerboe, 1978). The primary advantage
SUMPB/D 1-11 9/30/83
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of this method is that it allows simultaneous measurement of a large number of elements in a
small sample. In a study of environmental contamination by automotive lead, sampling times
were shortened by using a sampling technique in which lead-free porous graphite was used both
as the filter medium and as the electrode in the spectrometer. Lead concentrations of 1 to
10 pg/m8 were detected after a half-hour flow at 800 to 1200 ml/min through the filter.
More recent activities have focused attention on the inductively coupled plasma (ICP)
system as a valuable means of excitation and analysis (Garbarlno and Taylor, 1979). The ICP
system offers a higher degree of sensitivity with less analytical interference than is typical
of many of the other emission spectroscopic systems. Optical emission methods are inefficient
when used for analysis of a single element, since the equipment is expensive and a high level
of operator training is required. This problem is largely offset when analysis for several
elements is required, as is often the case for atmospheric aerosols. X-ray fluorescence (XF)
allows simultaneous identification of several elements, including lead, using a high-energy
irradiation source. With the X-ray tubes coupled with fluorescers, very little energy is
transmitted to the sample; thus sample degradation 1s kept to a minimum. Electron beams and
radioactive isotope sources have been used extensively as energy sources for XRF analysis.
X-ray emission induced by charged-particle excitation (proton-induced X-ray emission or
PIXE) offers an attractive alternative to the more common techniques. The excellent capabi-
lity of accelerator beams for X-ray emission analysis is partially due to the relatively low
background radiation associated with the excitation.
X-rad1ation is the basis of the electron microprobe method of analysis. When an intense
electron beam is incident on a sample, it produces several forms of radiation, Including
X-rays, whose wavelengths depend on the elements present in the material and whose Intensities
depend on the relative quantities of these elements. The method is unique 1n providing com-
positional information on individual lead particles, thus permitting the study of dynamic che-
mical changes and perhaps allowing improved source identification.
Isotope dilution mass spectrometry (IOMS) is the most accurate measurement technique
known at the present time. No other techniques serve more reliably as a comparative refer-
ence; 1t has been used for analyses of subnanogram concentrations of lead 1n a variety of sam-
ple types (Chow et al., 1969, 1974; Facchetti and Geiss, 1982; Hirao and Patterson, 1974;
Murozumi et al., 1969; Patterson et al., 1976; Rabinowitz et al., 1973). The isotoplc compo-
sition of lead peculiar to various ore bodies and crustal sources may also be used as a means
of tracing the origin of anthropogenic lead.
Colorimetrlc or spectrophotometry analysis for lead using dithizone (diphenylthiocarba-
zone) as the reagent has been used for many years. It was the primary method recommended by a
National Academy of Sciences (1972) report on lead, and the basis for the tentative method of
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testing for lead in the atmosphere by the American Society for Testing Materials (1975b).
Prior to the development of the IOMS method, colorlmetrlc analysis served as the reference by
which other methods were tested.
Analytical methods based on electrochemical phenomena are found in a variety of forms.
They are characterized by a high degree of sensitivity, selectivity, and accuracy derived from
the relationship between current, charge, potential, and time for electrolytic reactions in
solutions. Anodic stripping voltammetry (ASV) is a two step process in which the lead is pre-
concentrated onto a mercury electrode by an extended but selected period of reduction. After
the reduction step, the potential is scanned either linearly or by differential pulse to oxi-
dize the lead and allow measurement of the oxidation (stripping) current.
The majority of analytical methods are restricted to measurement of total lead and cannot
directly identify the various compounds of lead. Gas chromatography (GC) using the electron
capture detector has been demonstrated to be useful for organolead compounds. The use of
atomic absorption as the GC detector for organolead compounds has been described by De Jonghe
et al. (1981), while a plasma emission detector has been used by Estes et al. (1981). In ad-
dition, Messman and Rains (1981) have used liquid chromatography with an atomic absorption
detector to measure organolead compounds. Mass spectrometry may also be used with gas chroma-
tography (Mykytiuk et al., 1980).
1.5 SOURCES AND EMISSIONS
The history of global lead emissions has been assembled from chronological records of de-
position in polar snow strata, marine and freshwater sediments, and the annual rings of trees.
These records aid 1n establishing natural background levels of lead in air, soils, plants,
animals, and humans, and they document the sudden increase In atmospheric lead at the time of
the Industrial revolution, with a later burst during the 1920's when lead-alkyls were first
added to gasoline. Pond sediment analyses have shown a 20-fold increase in lead deposition
during the last 150 years (Figure 1-4), documenting not only the increasing use of lead since
the beginning of the Industrial revolution 1n western United States, but also the relative
fraction of natural vs. anthropogenic lead inputs. Other studies have shown the same magni-
tude of increasing deposition in freshwater marine sediments. The pond and marine sediments
also document the shift in isotoplc composition of atmospheric caused by increased commercial
use of the New Lead Belt in Missouri, where the ore body has an isotoplc composition substan-
tially different from other ore bodies of the world.
Perhaps the best chronological record is that of the polar ice strata of Murozuml et al.
(1969), which extends nearly three thousand years back in time (Figure 1-4). At the South
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1.0
Q.f
0.8
0.7
-j
$
3
H
z
ui
cc
s
0.6
0.6 —
3
U
0.4 —
1
< 0.3 -
OJ
0.1
1980
1760
1776
1826
192B
1975
1900
1800
1860
1876
YEAR
Figure 14. Chronological record of the relative Increase of lead in snow strata, pond
and lake sediments, marine sediments, arid tree rings. The data are expressed as a
ratio of the latest year of the record and should not be Interpreted to extend back in
time to natural or uncontaminated levels of lead concentration.
Source: Adapted from Muroiumi et el. (1969) (O I, Shlrahata et al. (1980) (~}, idgington
and Robbins (1976) (A), Ng and Patterson (1982) (A), and Rolfe (1974) (•).
Pole, Boutron (1982) observed a 4-fold Increase of lead In snow from 1957 to 1977 but saw no
¦Increase during the period 1927 to 1917. The author suggested the extensive atmospheric lead
pollution which began In the 1920's did not reach the South Pole until the aid-1950's. This
Interpretation agrees with that of Maenhaut et al. (1979), who found atmospheric concentra-
tions of lead of 0.000076 |ig/m9 at the same location. This concentration is about 3-fold
higher than the 0.000024 tig/*3 estimated by Patterson (1980) and Servant (1982) to be the
natural lead concentration In the atmosphere. In summary, 1t is likely that atmospheric lead
emissions have increased 2000-fold since the pre-Roman era, that even at this early tine the
atmosphere may have been contaminated by a factor of three over natural levels (Murozumi et
al. 1969), and that global atmospheric concentrations have increased dramatically since the
1920's.
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The history of global missions aay also be inferred from total production of lead.
The historical picture of lead production has been pieced together fro* many sources by Settle
and Patterson (1980) (Figure 1-5). Until the Industrial revolution, lead production was
determined largely by the ability or desire to mine lead for its silver content. Since that
time, lead has been used as an industrial product in its own right, anfl efforts to improve
smelter efficiency, including control of stack emissions and fugitive dusts, have made lead
production more economical. This improved efficiency is not reflected in the chronological
record because of atmospheric emissions of lead from many other anthropogenic sources,
especially gasoline combustion (see Section 5.3.3). From this knowledge of the chronological
record, it is possible to sort out contemporary anthropogenic emissions from natural sources
of atmospheric lead.
SPANISH PRODUCTION
OF SILVER
IN NEW WORLD
INDUSTRIAL
REVOLUTION
EXHAUSTION SILVER
OF ROMAN PRODUCTION
LEAD MINES IN GERMANY
INTRODUCTION
OF COINAGE
DISCOVERY OF
CUPELLATION
RISE AND FALL
OF ATHENS
ROMAN REPUBLIC
ANO EMPIRE
5500 6000 4600 4000 3600 3000 2600 2000 1600 1000 600
YEARS BEFORE PRESENT
Figure 1-6. The global lead production has changed historically in response to
major economic and political events. Increases In lead production (note log
scale) correspond approximately to historical increases In lead emissions shown
in Figure 5-1.
Source: Adapted from Settle and Patterson (1980).
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Lead enters the biosphere from lead-bearing minerals in the lithosphere through both
natural and man-made processes. Measurements of soil materials taken at 20-cm depths in the
continental United States show a median lead concentration of 15 to 16 pg Pb/g soil. In
natural processes, lead is first incorporated in soil in the active root zone, from which it
¦ay be absorbed by plants, leached into surface waters, or eroded into windborne dusts.
Calculations of natural contributions using geochenical information indicate that natural
sources contribute a relatively small amount of lead to the atmosphere. It has been estimated
from geochemical evidence that the natural particulate lead level is less than 0.0005 yg/m3
(National Academy of Sciences, 1980), and probably lower than the 0.300076 MS}/"3 measured at
the South Pole (Maenhaut et al., 1979). In contrast, average lead concentrations in urban
suspended particulate matter range as high as 6 pg/m3 {U.S. Environmental Protection Agency,
1979, 1978). Evidently, most of this urban particulate lead originates from man-made sources.
Lead occupies an important position 1n the U.S. economy, ranking fifth among all metals
in tonnage used. Approximately 85 percent of the primary lead produced in this country is
from native mines, although often associated with minor amounts of zinc, cadmium, copper,
bismuth, gold, silver, and other minerals (U.S. Bureau of Mines, 1972-1982). Missouri lead
ore deposits account for approximately 80 to 90 percent of the domestic production. Total
utilization averaged approximately 1.36x10® t/yr over the 10-year period, with storage bat-
teries and gasoline additives accounting for ~70 percent of total use. Certain products,
especially batteries, cables, plumbing, weights, and ballast, contain lead that is
economically recoverable as secondary lead. Lead in pigments, gasoline additives, ammunition,
foil, solder, and steel products is widely dispersed and therefore is largely unrecoverable.
Approximately 40-50 percent of annual lead production is recovered and eventually recycled.
Lead or its compounds may enter the environment at any point during mining, smelting,
processing, use, recycling, or disposal. Estimates of the dispersal of lead emissions into
the environment by principal sources Indicate that the atmosphere is the major initial
recipient. Estimated lead emissions to the atmosphere are shown in Table 1-1. Mobile and
stationary sources of lead emissions, although found throughout the nation, tend to be con-
centrated in areas of high population density, and near smelters. Figure 1-6 shows the ap-
proximate locations of major lead mines, primary and secondary smelters and refineries, and
alky! lead paints (International Lead Zinc Research Organization, 1982).
The majority of lead compounds found in the atmosphere result from leaded gasoline com-
bustion. Several reports indicate that transportation sources contribute over 80 percent of
the total atmospheric lead. Other mobile sources, including aviation use of leaded gasoline
and diesel and jet fuel combustion, contribute Insignificant lead emissions to the atmosphere.
Automotive lead emissions occur as PbBrCl in fresh exhaust particles. The fate of emit-
ted lead particles depends upon particle size. Particles initially formed by condensation of
SUHPB/D 1-16 9/30/83
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PRELIMINARY DRAFT
TABLE 1-1. ESTIMATED ATMOSPHERIC LEAD EMISSIONS FOR THE
UNITED STATES, 1981 AND THE WORLD
Annual
Percentage of
Annual
U.S.
U.S. Total
Global
Source Category
Emissions
Emissions
Emissions
(t/yr)
-------
I
*-*
00
¦ MINES (IS)
~ SMELTERS AND REFINERIES (7) '
O SECONDARY SMELTERS AND REFINERIES <561
• LEAD ALKYL PLANTS 14)
g
5
Figure 1-6. Locations of major lead operations in the United States.
Source: International Lead Zinc Research Organization (1982).
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PRELIMINARY DRAFT
(>10 M90 percent on a mass basis) of vehicular lead compounds are emit-
ted as inorganic particles (e.g., PbBrCl), some organolead vapors (e.g., lead alkyls) are also
emitted. The largest volume of organolead vapors arises from the manufacture, transport, and
handling of leaded gasoline. Such vapors are photoreactive, and their presence in local atmo-
spheres is transitory. Organolead vapors are most likely to occur in occupational settings
and have been found to contribute less than 10 percent of the total lead present in the atmo-
sphere.
The use of lead additives in gasoline, which increased in volume for many years, is now
decreasing as automobiles designed to use unleaded fuel constitute the major portion of the
automotive population. The decline in the use of leaded fuel is the result of two regulations
promulgated by the U.S. Environmental Protection Agency (F.R., 1973 Decembers). The first
required the availability of unleaded fuel for use in automobiles designed to meet federal
emission standards with lead-sensitive emission control devices (e.g., catalytic converters);
the second required a reduction or phase-down of the lead content in leaded gasoline. Compli-
ance with the phase-down of lead in gasoline has recently been the subject of proposed rule-
makings. The final action (F.R., 1982 October 29) replaced the present 0.5 g/gal standard for
the average lead content of all gasoline with a two-tiered standard for the lead content of
leaded gasoline. Under this proposed rule, refineries would be required to meet a standard of
1.10 g/gal for leaded gasoline while maintaining an average 0.5 g/gal for all gasoline.
The trend in lead content for U.S. gasolines is shown in Figure 1-7. Of the total gas-
oline pool, which includes both leaded and unleaded fuels, the average lead content has
decreased 63 percent, from an average of 1.62 g/gal in 1975 to 0.60 g/gal in 1981.
Data describing the lead consumed in gasoline and average ambient lead levels (composite
of maximum quarterly values) versus calendar year are plotted in Figure 1-8. The linear cor-
relation between lead consumed 1n gasoline and the composite maximum average quarterly ambient
average lead level is very good. Between 1975 and 1980, the lead consumed in gasoline
decreased 52 percent (from 165,577 metric tons to 78,679 metric tons) while the corresponding
composite maximum quarterly average of ambient lead decreased 51 percent (from 1.23 yg/ms to
0.60 pg/ms). This indicates that control of lead in gasoline over the past several years has
effected a direct decrease in peak ambient lead concentrations.
Furthermore, the equation in Figure 1-8 implies that the complete elimination of lead
from gasoline might reduce the composite average of the maximum quarterly lead concentrations
at these stations to 0.05 M9/m3» a level typical of concentrations reported for nonurban sta-
tions in the U.S.
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2.40
2.00
1
S
z
1
(0
3
U.
o
H
o
o
lii
1
IU
5
1.B0
1.00
0.80
0.00
LEADED FUEL
SALES-WEIGHTED TOTAL
QASOUNE POOL
(LEADED AND UNLEADED
"AVERAGE")
UNLEADED FUEL
±
1»71 1878 1077 1078 1878 1*0 1881 1882*
CALENDAR YEAR
Figure 1-7. Trtnd In laad contsnt of U.S. gasol!n«s, 1976-1982. (DuPont, 1982).
*1982 DATA ARE FORECASTS.
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AVERAGE Pb - 6.93 x 10* (Pb CONSUMED) + 0.06
• 1976
,•1980
0.20 0.40 0.60 0J0 1.00 1.20
COMPOSITE MAXIMUM QUARTERLY AVERAGE LEAD LEVELS, pg/m'
Figure 1-8. Relationship between lead consumed in gasoline and composite maximum
quarterly average lead levels, 1975-1980.
*1961 AND 1962 DATA ARE ESTIMATES.
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PRELIMINARY DRAFT
Solid waste incineration and combustion of waste oil are principal contributors of lead
emissions from stationary sources. The manufacture of consumer products such as lead glass,
storage batteries, and lead additives for gasoline also contributes significantly to station-
ary source lead emissions. Since 1970, the quantity of lead emitted from the metallurgical
industry has decreased somewhat because of the application of control equipment and the clos-
ing of several plants, particularly in the zinc and pyrometallurgical industries,
A new locus for lead emissions emerged in the mid-1960s with the opening of the "Viburnum
Trend" or "New Lead Belt" in southeastern Missouri. The presence of ten mines and three ac-
companying lead smelters in this area makes it the largest lead-producing district in the
world.
There is no doubt that atmospheric lead has been a component of the human environment
since the earliest written record of civilization. Atmospheric emissions are recorded in
glacial ice strata and pond and lake sediments. The history of global emissions seems
closely tied to production of lead by industrially oriented civilizations. Although the
amount of lead to the atmosphere emitted from natural sources is a subject of controversy,
even the most liberal estimate (25 x 103 t/year) is dwarfed by the global emissions from
anthropogenic sources (450 X 10? t/year). The contribution of gasoline lead to total atmo-
spheric emissions has remained high, at 85 percent, as emissions from stationary sources have
decreased at the same pace as from mobile sources. The decrease in stationary source emis-
sions is due primarily to control of stack emissions, whereas the decrease in mobile source
emissions is a result of switchover to unleaded gasolines. Production of lead in the
United States has remained steady at about 1.2 X 10® t/year for the past decade. The gasoline
additive share of this market has dropped from 18 to 9.5 percent during the period 1971 to
1981. The decreasing use of lead in gasoline is projected to continue through 1990.
1.6 TRANSPORT AND TRANSFORMATION
At any particular location and time, the concentration of lead found in the atmosphere
depends on the proximity to the source, the amount of lead emitted from sources, and the de-
gree of mixing provided by the motion of the atmosphere. At the source, lead emissions are
typically around'10,000 yg/m3, while lead values in city air are usually between 0.1 and 10
jjg/m3. These reduced concentrations are the result of dilution of effluent gas with clean air
and the removal of particles by wet or dry deposition. Characteristically, lead concentra-
tions are highest in confined areas close to sources and are progressively reduced by dilution
or deposition in districts more removed from sources. In parking garages or tunnels, atmo-
spheric lead concentrations can be ten to a thousand times greater than values measured near
roadways or in urban areas. In turn, atmospheric lead concentrations are usually about 2h
SUMPB/D 1-22 9/30/83
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PRELIMINARY ORAFT
times greater In the central city than in residential suburbs. Rural areas have even lower
concentrations. Particle size distribution stabilizes within a few hundred kilometers of the
sources, although atmospheric concentration continues to decrease with distance. Ambient
organolead concentrations decrease more rapidly than inorganic lead, suggesting conversion
from the organic to the inorganic phase during transport. Inorganic lead appears to convert
from lead halides and oxides to lead sulfates.
Lead is removed from the atmosphere by wet or dry deposition. The mechanisms of dry de-
position have been incorporated into models that estimate the flux of atmospheric lead to the
earth's surface. Of particular interest is deposition on vegetation surfaces, since this lead
may be incorporated into food chains. Between wet and dry deposition, it is possible to cal-
culate an atmospheric lead budget that balances the emission inputs with deposition outputs.
Particles in air streams are subject to the same principles of fluid mechanics as par-
ticles in flowing water. The first principle is that of diffusion along a concentration gra-
dient. If the airflow is steady and free of turbulence, the rate of mixing is determined by
the diffusivity of the pollutant. By making generalizations of windspeed, stability, and sur-
face roughness, it is possible to construct models using a variable transport factor called
eddy diffusivity (K), in which K varies in each direction, including vertically. There is a
family of K-theory models that describe the dispersion of particulate pollutants. The sim-
plest K-theory model produces a Gaussian plume, called such because the concentration of the
pollutant decreases according to a normal or Gaussian distribution in both the vertical and
horizontal directions. These models have some utility and are the basis for most of the air
quality simulations performed to date (Benarie, 1980). Another family of models is based on
the conservative volume element approach, where volumes of air are seen as discrete parcels
having conservative meteorological properties, (Benarie, 1980). The effect of pollutants on
these parcels is expressed as a mixing ratio. These parcels of air may be considered to move
along a trajectory that follows the advective wind direction. None of the models have been
tested for lead. All of the models require sampling periods of two hours or less in order for
the sample to conform to a well-defined set of meteorological conditions. In most cases, such
a sample would be below the detection limits for lead. The common pollutant used to test
models is SO^ which can be measured over very short, nearly instantaneous, time periods. The
question of whether gaseous $02 can be used as a surrogate for particulate lead in these
models remains to be answered. v
Dispersion not influenced by complex terrain features depends on emission rates and the
volume of clean air available for mixing. These factors are relatively easy to estimate and
some effort has been made to describe ambient lead concentrations which can result under
selected conditions. On an urban scale, the routes of transport can be inferred from an iso-
pleth, i.e., a plot connecting points of identical ambient concentrations. These plots always
show that lead concentrations are maximum where traffic density is highest.
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Dispersion beyond cities to regional and remote locations is complicated by the fact that
there are no monitoring network data from which to construct isopleths, that removal by
deposition plays a more important role with time and distance, and that emissions from many
different geographic locations sources converge. Dispersion from point sources such as
smelters and refineries is described with isopleths in the manner of urban dispersion,
although the available data are notably less abundant,
Trijonis et al. (1980) reported lead concentrations for seven sites in St. Louis,
Missouri. Values around the CBD are typically two to three times greater than those found in
the outlying suburbs in St. Louis County to the west of the city. The general picture is one
of peak concentrations within congested commercial districts which gradually decline in out-
lying areas. However, concentration gradients are not steep, and the whole urban area has
levels of lead above 0.5 pg/m?. Lead in the air decreases 2%-fold from maximum values in
center city areas to well populated suburbs, with a further 2-fold decrease in the outlying
areas. These modeling estimates are generally confirmed by measurement.
The 15 mines and 7 primary smelters and refineries shown in Figure 1-6 are not located in
urban areas. Most of the 56 secondary smelters and refineries are likewise non-urban. Con-
sequently, dispersion from these point sources should be considered separately, but in a man-
ner similar to the treatment of urban regions. In addition to lead concentrations in air,
concentrations in soil and on vegetation surfaces are often used to determine the extent of
dispersion away from smelters and refineries.
Beyond the immediate vicinity of urban areas and smelter sites, lead in air declines
rapidly to concentrations of 0.1 to 0.5 pg/m?. Two mechanisms responsible for this change are
dilution with clean air and removal by deposition.
Source reconciliation is based on the concept that each type of natural or anthropogenic
emission has a unique combination of elemental concentrations. Measurements of ambient air,
properly weighted during multivariate regression analysis, should reflect the relative amount
of pollutant derived from each of several sources (Stolzenberg et al., 1982). Sievering et
al. (1980) used the method of Stolzenberg et al. (1982) to analyze the transport of urban air
from Chicago over Lake Michigan. They found that 95 percent of the lead in Lake Michigan air
could be attributed to various anthropogenic sources, namely coal fly ash, cement manufacture,
iron and steel manufacture, agricultural soil dust, construction soil dust, and incineration
emissions. Cass and McRae (1983) used source rec^ciliation in the Los Angeles Basin to
interpret 1976 NFAM data based on emission profiles from several sources. Their chemical ele-
ment balance model showed that 20 to 22 percent of the total suspended particle mass could be
attributed to highway sources.
Harrison and Williams (1982) determined air concentrations, particle size distributions,
and total deposition flux at one urban and two rural sites in England. The urban site, which
SUMPB/D 1-24 9/30/83
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PRELIMINARY DRAFT
had no apparent industrial, commercial or municipal emission sources, had an air lead concen-
tration of 3.8 Mfl/m?. whereas the two rural sites were about 0.15 pg/m?. The average particle
size became smaller toward the rural sites, as the MMED shifted downward from 0.5 |jm to 0.1
pm.
Knowledge of lead concentrations in the oceans and glaciers provides some insight into
the degrees of atmospheric mixing and long range transport. Patterson and co-workers have
measured dissolved lead concentrations in sea water off the coast of California, in the
Central North Atlantic (near Bermuda), and in the Mediterranean. The profile obtained by
Schaule and Patterson (1980) is shown in Figure 1-9. Surface concentrations in the Pacific
(14 ng/kg) were found to be higher than those of the Mediterranean or the Atlantic, decreasing
abruptly with depth to a relatively constant level of 1 to 2 ng/kg. The vertical gradient was
found to be much less in the Atlantic. Below the mixing layer, there appears to be no differ-
ence between lead concentrations in the Atlantic and Pacific. These investigators calculated
that industrial lead currently is being added to the oceans at about 10 times the rate of in-
troduction by natural weathering, with significant amounts being removed from the atmosphere
by wet and dry deposition directly into the ocean. Their data suggest considerable contamina-
tion of surface waters near shore, diminishing toward the open ocean.
Investigations of trace metal concentrations (including lead) in the atmosphere in remote
northern and southern hemispheric sites have revealed that the natural sources for such atmos-
pheric trace metals include the oceans and the weathering of the earth's crust, while the
major anthropogenic source is particulate air pollution. Enrichment factors for concentra-
tions relative to standard values for the oceans and the crust were calculated; ninety percent
of the particulate pollutants in the global troposphere are injected in the northern hemi-
sphere (Robinson and Robbins, 1971). Since the residence times for particles in the tropo-
sphere are much less than the interhemispheric mixing time, it is unlikely that significant
amounts of particulate pollutants can migrate from the northern to the southern hemisphere via
the troposphere.
Murozumi et al. (1969) have shown that long range transport of lead particles emitted
from automobiles has significantly polluted the polar glaciers. They collected samples of
snow and ice from Greenland and the Antarctic (Figure 1-10). The authors attribute the gra-
dient increase after 1750 to the Industrial Revolution and the accelerated increase after 1940
to the increased use of lead alkyls in gasoline. The most recent levels found in the
Antarctic snows were, however, less than those found in Greenland by a factor of 10 or more.
Evidence from remote areas of the world suggests that lead and other fine particle com-
ponents are transported substantial distances, up to thousands of kilometers, by general
weather systems. The degree of surface contamination of remote areas with lead depends both
on weather influences and on the degree of air contamination. However, even in remote areas,
man's primitive activities can play an important role in atmospheric lead levels.
SUMPB/D 1-25 9/30/83
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PRELIMINARY DRAFT
1000
• DISSOLVED Pto
O PARTICULATE Pb
2000
3000
4000 ^ I
6000
0
4
CONCENTRATION, ng Pb/kg
Figure 1-9. Profile of lead concentrations in the
central northeast Pacific. Values below 1000 m are
an order of magnitude lower than reported by
Tatsumoto and Patterson {1963} and Chow and
Patterson (1966).
Source: Schaule and Patterson (1980).
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PRELIMINARY DRAFT
0.20
0 18
0 16
0.14
cr
0.12
0.10
o_
0.08
0.06
0.04
0.02
0
800
1750
18S0
1900
1950
h-B, A. D. H
AGE OF SAMPLES
Figure 1-10. Load concentration profile in snow
strata of Northern Greenland.
Source: Murozumi et al. (1969).
Whitby et al. (1975) placed atmospheric particles Into three different size regimes: the
nuclei mode (<0.1 |jm), the accumulation mode (0.1 to 2 pw)i and the large particle mode (>2
pm). At the source, lead particles are generally in the nuclei and large particle modes.
Large particles are removed by deposition close to the source and particles in the nuclei mode
diffuse to surfaces or agglomerate while airborne to form larger particles of the accumulation
mode. Thus it is in the accumulation mode that particles are dispersed great distances.
A number of studies have used gas absorbers behind filters to trap vapor-phase lead com-
pounds. Because it is not clear that all the lead captured in the backup traps is, in fact,
in the vapor phase in the atmosphere, "organic" or "vapor phase" lead is an operational
definition in these studies. Purdue et al. (1973) measured both particulate and organic lead
in atmospheric samples. They found that the vapor phase lead was about 5 percent of the total
lead in most samples. It is noteworthy, however, that in an underground garage, total lead
concentrations were approximately five times those in ambient urban atmospheres, and the
organic lead increased to approximately 17 percent.
Lead is emitted into the air from automobiles as lead halides and as double salts with
ammonium halides (e.g., PbBrCl • 2NH^C1). From mines and smelters, PbSO^, PbO-PbSO^, and PbS
appear to be the dominant species. In the atmosphere, lead is present mainly as the sulfate
SUMPB/D
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PRELIMINARY DRAFT
with minor amounts of halides. It is not completely clear just how the chemical composition
changes in transport.
The ratio of Br to Pb is often cited as an indication of automotive emissions. From the
mixtures commonly used in gasoline additives, the mass Br/Pb ratio should be about 0.386 if
there has been no fractionation of either element (Harrison and Sturges, 1983). However,
several authors have reported loss of halide, preferentially bromine, from lead salts in atmo-
spheric transport. Both photochemical decomposition and acidic gas displacement have been
postulated as mechanisms. The Br/Pb ratios maybe only crude estimates of automobile emissions;
this ratio would decrease with distance from the highway from 0.39 to 0.35 at less proximate
sites and 0.25 in suburban residential areas. Habibi et al. (1970) studied the composition of
auto exhaust particles as a function of particle size. Their main conclusions follow:
1. Chemical composition of emitted exhaust particles is related to particle size.
2. There is considerably more soot and carbonaceous material associated with fine-
mode particles than with coarse-mode particles. Particulate matter emitted
under typical driving conditions is rich in carbonaceous material.
3. Only small quantities of 2PbBrCl¦NH.Cl were found in samples collected at the
tailpipe from the hot exhaust gas. Lead-halogen molar ratios in particles of
less than 10 pm MMED indicate that much more halogen is associated with these
solids than the amount expected from the presence of 2PbBrCl'NH4C1.
Lead sulfide is the main constituent of samples associated with ore handling and fugitive
dust from open mounds of ore concentrate. The major constituents from sintering and blast
furnace operations appeared to be PbSO^ and PbO-PbSO^, respectively.
Before atmospheric lead can have any effect on organisms or ecosystems, it must be trans-
ferred from the air to a surface. For natural ground surfaces and vegetation, this process
may be either dry or wet deposition. Transfer by dry deposition requires that the particle
move from the main airstream through the boundary layer to a surface. The boundary layer is
defined as the region of minimal air flow immediately adjacent to that surface. The thickness
of the boundary layer depends mostly on the windspeed and roughness of the surface. Airborne
particles do not follow a smooth, straight path in the airstream. On the contrary, the path
of a particle may be affected by micro-turbulent air currents, gravitation, or its own iner-
tia. There are several mechanisms which alter the particle path sufficient to cause transfer
to a surface. These mechanisms are a function of particle size, windspeed, and surface char-
acteristics. Transfer from the main airstream to the boundary layer is usually by sedimenta-
tion or wind eddy diffusion. From the boundary layer to the surface, transfer may be by any
of the six mechanisms, although those which are independent of windspeed (sedimentation, in-
terception, Brownian diffusion) are more likely.
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PRELIMINARY DRAFT
Particles transported to a surface by any mechanism are said to have an effective de-
position velocity (V^) which is measured not by rate of particle movement but by accumulation
on a surface as a function of air concentration. Several recent models of dry deposition have
evolved from the theoretical discussion of Fuchs (1964) and the wind tunnel experiments of
Chamberlain (1966). The models of Slinn (1982) and Davidson et al. (1982) are particularly
useful for lead deposition. Slinn's model considers a multitude of vegetation parameters to
find several approximate solutions for particles in the size range of 0.1 to 1.0 h». estima-
ting deposition velocities of 0.01 to 0.1 cm/sec. The model of Davidson et al. (1982) is
based on detailed vegetation measurements and wind data to predict a of 0.05 to 1.0 cm/sec.
Deposition velocities are specific for each vegetation type. Both models show a decrease in
deposition velocity as particle size decrease down to about 0.1 to 0.2 pm; as diameter
decreases further from 0.1 to 0.001 deposition velocity increases (see Figure 6-1).
Several investigators have used surrogate surface devices to measure dry deposition
rates. The few studies available on deposition to vegetation surfaces show deposition rates
comparable to those of surrogate surfaces and deposition velocities in the range predicted by
the models discussed above (Table 1-2). These data show that global emissions are in approxi-
mate balance with global deposition.
Andren et al. (1975) evaluated the contribution of wet and dry deposition of lead in a
study of the Walker Branch Watershed in Oak Ridge, Tennessee, during the period June, 1973 -
July, 1974. The mean precipitation in the area is approximately 130 cm/yr. Wet deposition
contributed approximately 67 percent of the total deposition for the period.
The geochemical mass balance of lead in the atmosphere may be determined from quantita-
tive estimates of inputs and outputs. Inputs amount to 450,000 - 475,000 metric tons an-
nually (Table 1-1). . The amount of lead removed by wet deposition is approximately 208,000
t/yr (Table 1-3).
The deposition flux for each vegetation type shown on Table 1-3 totals 202,000. The
combined wet and dry deposition is 410,000 metric tons, which compares favorably with the es-
timated 450,000 - 475,000 metric tons of emissions.
Soils have both a liquid and solid phase, and trace metals are normally distributed be-
tween these two phases. In the liquid phase, metals may exist as free ions or as soluble com-
plexes with organic or inorganic 1igands. Organic ligands are typically humic substances such
as fulvic or humic acid, and the inorganic ligands may be iron or manganese hydrous oxides.
Since lead rarely occurs as a free ion in the liquid phase (Camerlynck and Kiekens, 1982), its
mobility in the soil solution depends on the availability of organic or inorganic ligands.
The liquid phase of soil often exists as a thin film of moisture in intimate contact with the
solid phase. The availability of metals to plants depends on the equilibrium between the
liquid and solid phase. In the solid phase, metals may be incorporated into crystalline
SUMPB/D 1-29 9/30/83
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PRELIMINARY DRAFT
TABLE 1-2. SUMMARY OF SURROGATE AND VEGETATION SURFACE DEPOSITION OF LEAD
Depositional Surface
Flux
ng Pb/cmf/day
Air Cone
ng/m?
Deposition Velocity
cm/sec
Reference
Tree leaves (Paris)
0.38
0.086
1
Tree leaves (Tennessee)
0.29-1,2
...
2
Plastic disk (remote
California)
0.02-0.08
13-31
0.05-0.4
3
Plastic plates
(Tennessee)
0.29-1.5
110
0.05-0.06
4
Tree leaves (Tennessee)
110
0.005
4
Snow (Greenland)
0.004
0.1-0.2
0.1
5
Grass (Pennsylvania)
...
590
0.2-1.1
6
Coniferous forest (Sweden) 0.74
21 -
0.41
7
1. Servant, 1975
2. llndberg et al., 1982
3. Elias and Davidson, 1980
4. Lindberg and Harriss, 1981
5. Davidson et al,, 1981c
6. Davidson et al., 1982
1. Lannefors et al., 1983
minerals of parent rock material and secondary clay minerals or precipitated as insoluble
organic or inorganic complexes. They may also be adsorbed onto the surfaces of any of these
solid forms. Of these categories, the most mobile form Is in soil moisture, where lead can
move freely into plant roots or soil microorganisms with dissolved nutrients. The least
mobile is parent rock material, where lead may be bound within crystalline structures over
geologic periods of time; intermediate are the lead complexes and precipitates. Trans-
formation from one form to another depends on the chemical environment of the soil. The water
soluble and exchangeable forms of metals are generally considered available for plant uptake
(Camerlynck and Kiekens, 1982). These authors demonstrated that in normal soils, only a small
fraction of the total lead is in exchangeable form (about 1 pg/jj) and none exists as free lead
ions. Of the exchangeable lead, 30 percent existed as stable complexes, 70 percent as labile
complexes.
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TABLE 1-3. ESTIMATED GLOBAL DEPOSITION OF ATMOSPHERIC LEAD
Deposition from Atmosphere
Mass Concentration Deposition
10" kg/yr 10-« g/kg 10! kg/yr
Wet
To oceans 4.1 0.4 164
To continents 1.1 0.4 44
Area Deposition rate Deposition
Dry 10*? km? 10-? q/ml/vr 10? kg/yr
To oceans, ice caps, deserts 405 0.2 89
Grassland, agricultural
areas, and tundra 46 0.71 33
Forests 59 1.5 80
Total dry: 202
Total wet: 208
Global: 410
Source: This report.
Atmospheric lead may enter the soil system by wet or dry deposition mechanisms. Lead
could be immobilized by precipitation as less soluble compounds [PbC03, Pb(P04)2], by ion ex-
change with hydrous oxides or clays, or by chelation with humic and fulvic acids. Lead im-
mobilization is more strongly correlated with organic chelation than with iron and managanese
oxide formation (Zimdahl and Skogerboe, 1977). If organic chelation is the correct model of
lead immobilization in soil, then several features of this model merit further discussion.
First, the total capacity of soil to immobilize lead can be predicted from the linear rela-
tionship developed by Zimdahl and Skogerboe (1977) (Figure 1-11) based on the equation:
N = 2.8 x 10"6 (A) + 1.1 x 10-5 (B) - 4.9 x lo"5
where N is the saturation capacity of the soil expressed in moles/g soil, A is the cation ex-
change capacity of the soil in meq/100 g soil, and B is the pH.
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PRELIMINARY DRAFT
The soil humus model also facilitates the calculation of lead in soil moisture using
values available iri the literature for conditional stability constants (K) with fulvic acid.
The values reported for log K are linear in the pH range of 3 to 6 so that interpolations in
the critical range of pH 4 to 5.5 are possible (Figure 1-11). Thus, at pH 4.5, the ratio of
complexed lead to ionic lead is expected to be 3.8 x 103. For soils of 100 yg/g, the ionic
lead in soil moisture solution would be 0.03 pg/g-
6.0
X
IS
K
£
o
2
<
o
z
0
1
4
(A
pH = 8
pH - 6
pH - 4
SO 78
CEC. mcq/100 g
Figure 1-11. Variation of lead saturation capacity with cation exchange
capacity in soil at selected pH values.
Source: Data from Zimdahl and Skogerboe (1977).
It is also important to consider the stability constant of the Pb-FA complex relative to
other metals. Schnitzer and Hansen (1970) showed that at pH 3, Fe3+ is the most stable in
the sequence F«?+ > Al?+ > Cu1* > Ni 2+ > Co2+ > Pb2+ > Ca2+ > Zn2* > Mn2+ > Mg2+. At pH
5, this sequence becomes NiI+ = Co5?* > Pb2+ > Cu2+ > Zn2+ = Mn2+ > Ca2+ > Mg2+. This
»eans that at normal soil pH levels of 4.5 to 8, lead is bound to FA ~ HA in preference to
many other metals that are known plant nutrients (Zn, Mn, Ca, and Mg).
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PRELIMINARY DRAFT
Lead does not pass easily to ground or surface water. Any lead dissolved from primary
lead sulfide ore tends to combine with carbonate or sulfate ions to form insoluble lead car-
bonate or lead sulfate, or be absorbed by ferric hydroxide. An outstanding characteristic of
lead is its tendency to form compounds of low solubility with the major anions of natural
water. The hydroxide, carbonate, sulfide, and more rarely the sulfate may act as solubility
controls in precipitating lead from water. The amount of lead that can remain in solution is
a function of the pH of the water and the dissolved salt content. A significant fraction of
the lead carried by river water may be in an undissolved state. This insoluble lead can con-
sist of colloidal particles in suspension or larger undissolved particles of lead carbonate,
-oxide, -hydroxide, or other lead compounds incorporated in other components of particulate
lead from runoff; it may occur either as sorbed ions or surface coatings on sediment mineral
particles or be carried as a part of suspended living or nonliving organic matter.
The bulk of organic compounds in surface waters originates from natural ,sources.
(Neubecker and Allen, 1983). The humic and fulvic acids that are primary completing agents in
soils are also found in surface waters at concentrations from 1 to 5 mg/1, occasionally ex-
ceeding 10 mg/1. The presence of fulvic acid in water has been shown to increase the rate of
solution of lead sulfide 10 to 60 times over that of a water solution at the same pH that did
not contain fulvic acid. At pH values near 7, soluble lead-fulvic acid complexes are present
in solution.
The transformation of inorganic lead, especially in sediment, to tetramethyHead (TML)
has been observed and biomethylation has been postulated. However, Reisinger et al. (1981)
have reported extensive studies of the methylation of lead in the presence of numerous
bacterial species known to alkylate mercury and other heavy metals. In these experiments no
biological methylation of lead was found under any condition.
Lead occurs in riverine and estuarial waters and alluvial deposits. Concentrations of
lead in ground water appear to decrease logarithmically with distance from a roadway. Rain-
water runoff has been found to be an important transport mechanism in the removal of lead from
a roadway surface in a number of studies. Apparently, only a light rainfall, 2 to 3 mm, is
sufficient to remove 90 percent of the lead from the road surface to surrounding soil and to
waterways. The lead concentrations in off-shore sediments often show a marked increase
corresponding to anthropogenic activity in the region. An average anthropogenic flux of 72
mg/m2'yr, of which 27 mg/mz*yr could be attributed to direct atmospheric deposition. Prior to
1650, the total flux was 12 mg/m?*yr, so there has been a 6-fold increase since that time. Ng
and Patterson (1982) found prehistoric fluxes of 1 to 7 mg Pb/m2*yr to three offshore basins
in southern California, which have now increased 3 to 9-fold to 11 to 21 mg/m?-yr. Much of
this lead is deposited directly from sewage outfalls, although at least 25 percent probably
comes fro® the atmosphere.
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PRELIMINARY DRAFT
The deposition of lead on the leaf surfaces of plants where the particles are often re-
tained for a long time can be important. Several studies have shown that plants near roadways
exhibit considerably higher levels of lead than those farther away. Rainfall does not gene-
rally remove the deposited particles. Animals or humans consuming the leafy portions of such
plants can be exposed to higher than normal levels of lead. The particle deposition on leaves
has led some investigators to stipulate that lead may enter plants through the leaves. Arvik
and Zimdahl (1974) have shown that entry of ionic lead through plant leaves is of minimal
importance. Using the leaf cuticles of several types of plants essentially as dialysing mem-
branes, they found that even high concentrations of lead ions would not pass through the cuti-
cles into distilled water on the opposite side.
1.7 ENVIRONMENTAL CONCENTRATIONS AND POTENTIAL PATHWAYS TO HUMAN EXPOSURE
In general, typical levels of human lead exposure may be attributed to four components of
the human environment: Inhaled air, dusts of various types, food and drinking water. A base-
line level of potential human exposure is determined for a normal adult eating a typical diet
and living 1n a non-urban community. This baseline exposure is deemed to be unavoidable by
any reasonable means. Beyond this level, additive exposure factors can be determined for
other environments (urban, occupational, smelter communities), for certain habits and activi-
ties (smoking, drinking, pica, and hobbies), and for variations due to age, sex, or socio-
economic status.
1.7.1 Lead in Air
Ambient airborne lead concentrations may influence human exposure through direct inhala-
tion of lead-containing particles and through ingestion of lead which has been deposited from
the air onto surfaces. Our understanding of the pathways to human exposure is far from com*
plete because most ambient measurements were not taken 1n conjuctlon with studies of the con-
centrations of lead in man or in components of his food chain.
The most complete set of data on ambient air concentrations my be extracted from the
National filter. Analysis Network (NFAN) and Its predecessors. In remote regions of the world,
air concentrations are two or three orders of magnitude lower than In urban areas, lending
credence to estimates of the concentrations of natural lead in the atmosphere. In the context
of this data base, the conditions which modify ambient air, as measured by the monitoring net-
works, to air inhaled by humans cause changes in particle size distributions, changes with
vertical distance above ground-, and differences between Indoor and outdoor concentrations.
The wide range of concentration is apparent from Table 1-4, which summarizes data ob-
tained from numerous independent measurements. Concentrations vary from 0.000076 pg/m3 in
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PRELIMINARY ORAFT
TABLE 1-4. ATMOSPHERIC LEAD IN URBAN, RURAL, AND REMOTE AREAS OF THE WORLD3
^.11,111111111, , l. I, I "-»» » ¦ I I II ¦ ¦' !»»¦ I-
Location Sampling Period Lead conc. (pg/m3) Reference
Urban
Miami
1974
1.3
HASL, 1975
New York
1978-79
1.1
see Table 7-3
Boston
1978-79
0.8
see Table 7-3
St, Louis
1973
1.1
see Table 7-3
Houston
1978-79
0.9
see Table 7-3
Chicago
1979
0.8
see Table 7-3
Salt Lake City
1974
0.89
HASL, 1975
Los Angeles
1978-79
1.4
see Table 7-3
Ottowa
1975
1.3
NAPS, 1975
Toronto
1975
1.3
NAPS, 1975
Montreal
1975
2.0
NAPS, 1975
Berlin
1966-67
3.8
Blokker, 1972
Vienna
1970
2.9
Hartl and Resch, 1973
Zurich
1970
3.8
HSflger, 1973
Brussels
1978
0.5
Roels et al., 1980
Turin
1974-79
4.5
Facchetti and Geiss, 1982
Rome
1972-73
4.5
Colacino and Lavagnini, 1974
Paris
1964
4.6
Blokker, 1972
Rio de Janeiro
1972-73
0.8
Branquinho and Robinson, 197<
Rural
New York Bight
1974
0.13
Duce et al., 1975
Framingham, MA
1972
0.9
O'Brien et al., 1975
Chadron, NE
1973-74
0.045
Struempler, 1975
United Kingdom
1972
0.13
Cawse, 1974
Italy
1976-80
0.33
Facchetti and Geiss, 1982
Belgium
1978
0.37
Roels et al. 1980
Remote
White Mtn., CA
1969-70
0.008
Chow et al., 1972
High Sierra, CA
1976-77
0.021
Elias and Davidson, 1980
Olympic Nat. Park, WA
1980
0.0022
Davidson et al., 1982
Antarctica
1971
0.0004
Duce, 1972
South Pole
1974
0.000076
Maenhaut et al., 1979
Thule, Greenland
1965
0.0005
Murozumi et al., 1969
Thule, Greenland
1978-79
0.008
Heldam, 1981
Prins Christian-
sund, Greenland
1978-79
0.018
Heidam, 1981
Dye 3, Greenland
1979
0.00015
Davidson et al., 1981c
Eniwetok, Pacific Ocean
1979
0.00017
Settle and Patterson, 1982
Kuajung, Nepal
1979
0.00086
Davidson et al., 1981b
Bermuda
1973-75
0.0041
Duce et al., 1976
Spitsbergen
1973-74
0.0058
Larssen, 1977
aA11 references listed as cited in Nriagu (1978b).
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remote areas to over 10 pg/m3 near sources such as smelters. Many of the remote areas are far
from human habitation and therefore do not reflect human exposure. However, a few of the
regions characterized by small lead concentrations are populated by individuals with primitive
lifestyles; these data provide baseline airborne lead data to which modern American lead expo-
sures can be compared.
The remote area concentrations reported in Table 1-4 do not necessarily reflect natural,
preindustrial lead. Murozumi et al. (1969) and Ng and Patterson (1981) have measured a 200-
fold increase in the lead content of Greenland snow over the past 3000 years. The authors
state that this lead originates in populated mid-latitude regions, and is transported over
thousands of kilometers through the atmosphere to the Arctic. All of the concentrations in
Table 1-4, including values for remote areas, have been influenced by anthropogenic lead emis-
sions.
The data from the Air Filter networks show both the maximum quarterly average to reflect
compliance of the station to the ambient airborne standard (1.5 pg/m3), and quarterly aver-
ages to show trends at a particular location. The number of stations complying with the stan-
dard has increased, the quarterly averages have decreased, and the maximum 24-hour values ap-
pear to be smaller since 1977.
It seems likely that the concentration of natural lead in the atmosphere is between
0.00002 and 0.00007 pg/m3. A value of 0.00005 will be used for calculations regarding the
contribution of natural air lead to total human uptake.
The effect of the 1978 National Ambient Air Quality Standard for Lead has been to reduce
the air concentration of lead in major urban areas. Similar trends may also be seen in urban
areas of smaller population density. There are many factors which can cause differences
between the concentration of lead measured at a monitoring station and the actual inhalation
of air by humans. Air lead concentrations usually decrease with vertical and horizontal dis-
tance from emission sources, and are generally lower indoors than outdoors.
New guidelines for placing ambient air lead monitors went into effect in July, 1981
(F.R., 1981 September 3). "Microscale" sites, placed between 5 and 15 meters from thorough-
fares and 2 to 7 meters above the ground, are prescribed, but until now few monitors have been
located that close to heavily travelled roadways. Many of these microscale sites might be ex-
pected to show higher lead concentrations than measured at nearby middlescale urban sites, due
complex. Our understanding of the complex factors affecting the vertical distribution of air-
borne lead is extremely limited, but the data indicate that air lead concentrations are pri-
marily a function of distance from the source, whether vertical or horizontal.
Because people spend much of their time indoors, ambient air data may not accurately
indicate actual exposure to airborne lead. Some studies show smaller indoor/outdoor ratios
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during the winter, when windows and doors are tightly closed. Overall, the data suggest
indoor/outdoor ratios of 0.6-0.8 are typical for airborne lead in houses without air con-
ditioning. Ratios in air conditioned houses are expected to be in the range of 0.3-0.5
(Yocum, 1982). Even detailed knowledge of indoor and outdoor airborne lead concentrations at
fixed locations may still be insufficient to assess human exposure to airborne lead. The
study of Tosteson et al. (1982) included measurement of airborne lead concentrations using
personal exposure monitors, carried by Individuals going about their day-to-day activities.
In contrast to the lead concentrations of 0.092 and 0.12 |jg/ms at fixed locations, the average
personal exposure was 0.16 Mg/">s- The authors suggest the inadequacy of using fixed monitors
at either indoor or outdoor locations to assess exposure.
Much of the lead in the atmosphere is transferred to terrestrial surfaces where 1t is
eventually passed to the upper layer of the soil surface. Crustal lead concentrations In soil
range from less than 10 to greater than 70 ug/g- The range of values probably represent
natural levels of lead in soil, although there may have been some contamination with anthro-
pogenic lead during collection and handling.
1.7.2 Lead in Soil and Dust
Studies have determined that atmospheric lead is retained in the upper two centimeters of
undisturbed soil, especially soils with at least 5 percent organic matter and a pH of 5 or
above. There has been no general survey of this upper 2 cm of the soil surface in the United
States, but several studies of lead in soil near roadsides and smelters and a few studies of
lead in soil near old houses with lead-based paint can provide the backgound information for
determining potential human exposures to lead from soil. Because lead is immobilized by the
organic component of soil, the concentration of anthropogenic lead in the upper 2 cm is deter-
mined by the flux of atmospheric lead to the soil surface. Near roadsides, this flux is
largely by dry deposition and the rate depends on particle size and concentration. In gen-
eral, deposition flux drops off abruptly with increasing distance from the roadway. This
effect is demonstrated in studies which show surface soil lead decreases exponentially up to
25 a from the edge of the road. Roadside soils may contain atmospheric lead from 30 to 2000
mg/g in excess of natural levels within 25 meters of the roadbed, all in the upper layer of
the soil profile.
Near primary and secondary smelters, lead in soil decreases exponentially within a 5-10
km zone around the smelter complex. Soil lead contamination varies with the smelter emission
rate, length of time the smelter has been in operation, prevailing windspeed and direction,
regional climatic conditions, and local topography.
Urban soils may be contaminated from a variety of atmospheric and non-atmospheric
sources. The major sources of soil lead seem to be paint chips from older houses and deposi-
tion from nearby highways. Lead in soil adjacent to a house decreases with distance; this may
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PRELIMINARY DRAFT
be due to paint chips or to dust of atmospheric origin washing fro# the rooftop (Wheeler and
Rolfe, 1979).
A definitive study which describes the source of soil lead was reported by Gutson et al.
(1981) for soils in the vicinity of Adelaide, South Australia. In an urban to rural transect,
stable lead isotopes were measured in the top 10 cm of soils over a 50 km distance. By their
isotopic compositions, three sources of lead were identified: natural, non~automotive in-
dustrial lead from Australia, and tetraethyl lead manufactured in the United States. The re-
sults indicated most of the soil surface lead originated from leaded gasoline. Lead may be
found in inorganic primary minerals, on humic substances, complexed with Fe-Mn oxide films, on
secondary minerals or in soil moisture. All of the lead in primary minerals is natural and is
bound tightly within the crystalline structure of the minerals. The lead on the surface of
these minerals is leached slowly into the soil moisture. Atmospheric lead forms complexes
with humic substances or on oxide films, that are in equilibrium with soil moisture, although
the equilibrium strongly favors the complexing agents. Except near roadsides and smelters,
only a few MS of atmospheric lead have been added to each gram of soil. Several studies in-
dicate that this lead is available to plants and that even with small amounts of atmospheric
lead, about 75 percent of the lead in soil moisture is of atmospheric origin.
Lead on the surfaces of vegetation may be of atmospheric origin. In internal tissues,
lead maybe a combination of atmospheric and soil origin. As with soils, lead on vegetation
surfaces decreases exponentially with distance away from roadsides and smelters. This de-
posited lead is persistent. It is neither washed off by rain nor taken up through the leaf
surface. Lead on the surface of leaves and bark is proportional to air lead concentrations
and particle size distributions. Lead in internal plant tissues is directly related to lead
in soil.
1.7.3 Lead in Food
In a study to determine the background concentrations of lead and other metals in agri-
cultural crops, the Food and Drug Administration (Wolnik et al., 1983), in cooperation with
the U.S. Department of Agriculture and the U.S. Environmental Protection Agency, analyzed over
1500 samples of the post common crops taken from a cross section of geographic locations.
.Collection sites were remote from mobile or stationary sources of lead. Soil lead concentra-
tions were within the normal range (8-25 Mg/g) of U.S. soils. The concentrations of lead in
crops are shown as "Total" concentrations on Table 1-5. The total concentration data should
probably be seen as representing the lowest concentrations of lead in food available to
Americans. The data on these ten crops suggest that root vegetables have lead concentrations
between 0.0046 and 0.009 pg/g, all soil lead. Aboveground parts not exposed to significant
amounts of atmospheric deposition (sweet corn and tomatoes) have less lead internally. If it
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PRELIMINARY DRAFT
1s assumed that this sane concentration is the internal concentration for aboveground parts
for other plants, it is apparent that five crops have direct atmospheric deposition in pro-
portion to surface area and estimated duration of exposure. The deposition rate of 0.04
ng/cm2*day in rural environments could account for these amounts of direct atmospheric lead.
TABLE 1-5. BACKGROUND LEAD IN BASIC FOOD CROPS AND MEATS
(pg/g fresh weight)
Crop
Natural
Pb
Indirect
Atmospheric
Direct
Atmospheric
Total*
Wheat
0.0015
0.0015
0.034
0.037
Potatoes
0.0045
0.0045
—
0.009
Field corn
0.0015
0.0015
0.019
0.022*
Sweet corn
0.0015
0.0015
~
0.003
Soybeans
0.021'
0.021
--
0.042
Peanuts
0.050
0.050
—
0.10Q
Onions
0.0023
0.0023
--
0.0046*
Rice
0.0015
0.0015
0.004
0.007*
Carrots
0.0045
0.0045
—
0.009*
Tomatoes
0.001
0.001
—
0.002*
Spinach
0.0015
0.0015
0.042
0.045*
Lettuce
0.0015
0.0015
0.010
0.013
Beef (muscle)
0.0002
0.002
0.02
0.02**
Pork (muscle)
0.0002
0.002
0.06
0.06**
^except as indicated, data are from Wolnick et al. (1983)
'preliminary data provided by the Elemental Analysis Research Center, Food and Drug
Administration, Cincinnati, OH
**data from Penumarthy et al. (1980)
Lead in food crops varies according to exposure to the atmosphere and in proportion to the ef-
fort taken to separate husks, chaff, and hulls from edible parts during processing for human
or animal consumption. Root parts and protected aboveground parts contain natural lead and
Indirect atmospheric lead, both derived from the soil. For exposed aboveground parts, any
lead in excess of the average of unexposed aboveground parts is considered to have been
directly deposited from the atmosphere.
1.7.4 Lead in Water
Lead occurs in untreated water 1n either dissolved or particulate form. Dissolved lead is
operationally defined as that which passes through a 0.45 pm membrane filter. Because atmos-
pheric lead in rain or snow is retained by soil, there 1s little correlation between lead in
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precipitation and lead in streams that drain terrestrial watersheds. Rather, the important
factors seen to be the chemistry of the stream (pH and hardness) and the volume of the stream
flow. For groundwater, chemistry is also Important, as is the geochemical composition of the
water-bearing bedrock.
Streams and lakes are influenced by their water chemistry and the lead content of their
sediments. At neutral pH, lead moves from the dissolved to particulate form and the particles
eventually pass to sediments. At low pH, the reverse pathway is generally the case. Hard-
ness, which 1s a combination of the Ca and Mg concentration, can also influence lead concen-
trations. At higher concentrations of Ca and Mg, the solubility of lead decreases. Municipal
and private wells typically have a neutral pH and somewhat higher than average hardness. Lead
concentrations are not influenced by acid rain, surface runoff or atmospheric deposition.
Rather, the primary determinant of lead concentration 1s the geochemical makeup of the bedrock
that is the source of the water supply. Ground water typically ranges from 1 to 100 pg Pb/1
(National Academy of Sciences, 1980).
Whether from surface or ground water supplies, municipal waters undergo extensive chem-
ical treatment prior to release to the distribution system. Although there is no direct ef-
fort to remove lead from the water supply, some treatments, such as flocculation and sedimen-
tation, may inadvertently remove lead along with other undesirable substances. On the other
hand, chemical treatment to soften water increases the solubility of lead and enhances the
possibility that lead1 will be added to water as it passes through the distribution system.
For samples taken at the household tap, lead concentrations are usually higher in the initial
volume (first daily flush) than after the tap has been running for some time. Water standing
in the pipes for several hours is intermediate between these two concentrations. (Sharrett et
al., 1982; Worth et al., 1981).
1.7.5 Baseline Exposures to Lead
Lead concentrations in environmental media that are in the pathway to human consumption
are summarized on Table 1-6. Because natural lead is generally three to four orders of magni-
tude lower than anthropogenic lead in ambient rural or urban air, all atmospheric contri-
butions of lead are considered to be of anthropogenic origin. Natural soil lead typically
ranges from 10 to 30 MS/fl. but much of this is tightly bound within the crystalline matrix of
soil minerals at normal soil pHs of 4 to 8. Lead in the organic fraction of soil is part
natural and part atmospheric. The fraction derived from fertilizer 1s considered to be
minimal. In undisturbed rural and remote soils, the ratio of natural to atmospheric lead is
about 1:1, perhaps as high as 1:3. This ratio persists through soil moisture and into in-
ternal plant tissues.
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TABLE 1-6. SUMMARY OF ENVIRONMENTAL CONCENTRATIONS OF LEAD
Medi um
Natural
Lead
Atmospheric
Lead
Total
Lead
Air urban (>jg/i*3) 0.00005
0.8
0.2
0.8
0.2
rural (pg/»3) 0.00005
Soil Total (jig/fl) 8-25
Food Crops (pg/g) 0.0025
Surface water (yg/g) 0.00002
Ground water (pg/g) 0.003
8-25
0.005
0.027
3.0
15.0
0.03
0.005
0.003
In tracking air lead through pathways to hunan exposure, it is necessary to distinguish
between atmospheric lead that has passed through the soil, called indirect atmospheric here,
and atmospheric lead that has deposited directly on crops or water. Because indirect atmos-
pheric lead will remain in the soil for many decades, this source is insensitive to projected
changes in atmospheric lead concentrations.
Initially, a current baseline exposure scenario is described for an individual with a
minimum amount of daily lead consumption. This person would live and work in a rwnurtoan en-
vironment, eat a normal diet of food taken from a typical grocery shelf, and would have no
habits or activities that would tend to increase lead exposure. Lead exposure at the baseline
level is considered unavoidable without further reductions of lead in the atmosphere or in
canned foods. Most of the baseline lead is of anthropogenic origin.
To arrive at a minimum or baseline exposure for humans, it is necessary to begin with the
environmental components, air, soil, food crops and water, that are the major sources of lead
consumed by humans (Table 1-6). These components are measured frequently, even monitored
routinely in the case of air, so that much data are available on their concentrations. But
there are several factors which modify these components prior to actual human exposure: We do
not breathe air as monitored at an atmospheric sampling station; we may be closer to or
farther from the source of lead than is the monitor; we nay be inside a building, with or
without filtered air; water we drink does not come directly from a stream or river, but often
has passed through a chemical treatment plant and a distribution system. A similar type of
processing has modified the lead levels present in our food.
Besides the atmospheric lead in environmental components, there are two other industrial
components which contribute to this baseline of human exposure: paint pigments and lead
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solder. Solder contributes directly to the human diet through canned food and copper water
distribution systems. Paint and solder are also a source of lead-bearing dusts. The most
common dusts in the baseline human environment are street dusts and household dusts. They
originate as emissions from mobile or stationary sources, as the oxidation products of surface
exposure, or as products of frictional grinding processes. Ousts are different from soil in
that soil derives from crustal rock and typically has a lead concentration of 10 to 30 Mi/fl.
whereas dusts come from both natural and anthropogenic sources and vary from 1000 to 10,000
Mg/fl-
The route by which many people receive the largest portion of their daily lead intake is
via foods. Several studies have reported average dietary lead intakes in the range 100 to 500
pg/day for adults, with individual diets covering a much greater range (Nutrition Foundation,
1982). The sources of lead in plants and animals are air, soil, and untreated waters (Figure
1-13). Food crops and livestock contain lead in varying proportions from the atmosphere and
natural sources. From the farm to the dinner table, lead is added to food as it is harvested,
transported, processed, packaged, and prepared. The sources of this lead are dusts of atmos-
pheric and industrial origin, metals used in grinding, crushing, and sieving, solder used in
packaging, and water used in cooking. Pennington (1983) has identified 234 typical food cate-
gories for Americans grouped into eight age/sex groups. These basic diets are the foundation
for the Food and Orug Administration's revised Total Diet Study, often called the "Market
Basket Study", beginning in April, 1982. The diets used for this discussion include food,
beverages, and drinking water for the 2-year-old child, the adult female 25 to 30 years of
age, and the adult male 25 to 30 years of age.
Milk and foods are treated separately from water and beverages because solder and atmos-
pheric lead contribute significantly to each of these later dietary components (Figure 1-1).
Between the field and the food processor, lead is added to food crops. It Is assumed
that this lead is all of direct atmospheric origin. Direct atmospheric lead can be deposited
directly on food materials by dry deposition, or it can be lead on dust which has collected on
other surfaces, then transferred to foods. For the purposes of this discussion, it 1s not
necessary to distinguish between these two forms, as both are a function of air concentration.
For some of the food items, data are available on lead concentrations just prior to fil-
ling of cans. In the case where the food product has not undergone extensive modification
(e.g. cooking or added ingredients), the added lead was most likely derived from the atmos-
phere or from the machinery used to handle the product.
From the 'time a product is packaged in bottles, cans, or plastic containers until it is
opened in the kitchen, it may be assumed that no food item receives atmospheric lead. Most of
the lead which is added during this stage comes from the solder used to seal some types of
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PRELIMINARY DRAFT
TABLE 1-7. SUMMARY BY AGE AND SEX OF ESTIMATED AVERAGE LEVELS
OF LEAD INGESTED FROM MILK AND FOODS
Dietary consumption Lead consumption
Co/day) ug/day
2-yr-old Adult Adult 2-yr-old Adult Adult
Child Female Male ^9 Pb/g* Child Female Male
A. Dairy
381
237
344
0.013
5.0
3.1
4.5
B. Meat
113
169
288
0.036
4.1
6.1
10.4
C. Food crops
260
350
505
0.022
5.7
7.7
11.1
D. Canned food
58
68
82
0.24
13.9
16.3
19.7
Total
812
824
1219
28.7
33.2
45.6
"Weighted average lead concentration in foods from Table 7-15 in Chapter 7 of this document,
cans. Estimates by the Food and Drug Administration, prepared in cooperation with the
National Food Processors Association, suggest that lead 1n solder contributes more than 66
percent of the lead in canned foods where a lead solder side seam was used. This lead 1s
thought to represent a contribution of 20 percent to the total lead consumption 1n foods.
The contribution of the canning process to overall lead levels in albacore tuna has been
reported by Settle and Patterson (1980). The study showed that lead concentrations in canned
tuna are elevated above levels in frfesh tuna by a factor of 4000. Nearly all of the increase
results from leaching of the lead from the soldered seam of the can; tuna front an unsoldered
can is elevated by a factor of only 20 compared with tuna fresh from the sea.
It is assumed that no further lead is added to food packaged in plastic or paper con-
tainers, although there are no data to support or reject this assumption.
Studies that reflect contributions of lead added during kitchen preparation showed that
lead 1n acidic foods stored refrigerated in open cans can Increase by a factor of 2 to 8 in
five days if the cans have a lead-soldered side seam not protected by an interior lacquer
coating (Capar, 1978). Comparable products in cans with the lacquer coating or in glass jars
showed little or no Increase.
As a part of Its program to reduce the total lead intake by children (0-5 years) to less
than 100 yg/day by 1988, the Food and Drug Administration estimated lead intakes for Individ-
ual children in a large-scale food consumption survey (Beloian and McDowell, 1981). Between
1973 and 1978, intensive efforts were made by the food industry to remove sources lead from
infant food items. By 1980, there had been a 47 percent reduction in the age group 0-5 months
and a 7 percent reduction for 6-23 months. Most of this reduction was accomplished by the
removal of soldered cans used for infant formula.
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Because the Food and Drug Administration is actively pursuing programs to remove lead
from adult foods, it is probable that there will be a decrease in total dietary lead consump-
tion over the next decade independent of projected decreases in atmospheric lead concentra-
tion. With both sources of lead minimized, the lowest reasonable estimated dietary lead con-
sumption would be 10-15 yg/day for adults and children. This estimate assumes about 90 per-
cent of the direct atmospheric, solder lead and lead of undetermined origin would be removed
from the diet, leaving 8 m9 from these sources and 3 pg of natural and indirect atmospheric
lead.
There have been several studies in North America and Europe of the sources of lead in
drinking water. The baseline concentration of water across the whole United States is taken
to be 10 mq/1. although 6-8 pg/1 are often cited in the literature for specific locations. A
recent study in Seattle, WA by Sharrett et al. (1982) showed that the age of the house and the
type of plumbing determined the lead concentration in tap water. Standing water from houses
newer than five years (copper pipes) averaged 31 while houses less than 18 months old
averaged about 70 pg/1. Houses older than five years and houses with galvanized pipe averaged
less than 6 pg/1. The source of the water supply, the length of the pipe, and the use of
plastic pipes in the service line had little or no effect on the lead concentrations. It ap-
pears certain that the source of lead in new homes with copper pipes is the solder used to
join these pipes, and that this lead is eventually worn away with age.
Ingestion, rather than inhalation, of dust particles appears to be the greater problem in
the baseline environment, especially ingestion during meals and playtime activity by small
children. Although dusts are of complex origin, they may be conveniently placed into a few
categories relating to human exposure. Generally, the most convenient categories are house-
hold dusts, soil dust, street dusts, and occupational dusts. It is a characteristic of dust
particles that they accumulate on exposed surfaces and are trapped 1n the fibers of clothing
and carpets. Two other features of dusts are important. First, they must be described in
both concentration and amount; the concentration of lead in street dust may be the same in a
rural and urban environment, but the amount of dust may differ by a wide margin. Secondly,
each category represents some combination of sources. Household dusts contain some atmospher-
ic lead, some paint lead, and some soil lead; street dusts contain atmospheric, soil, and oc-
casionally paint lead. For the baseline human exposure, it is assumed that workers are not
exposed to occupational dusts, nor do they live in houses with interior leaded paints. Street
dust, soil dust, and some household dust are the primary sources for baseline potential human
exposure.
In considering the impact of street dust on the human environment, the obvious question
arises as to whether lead in street dust varies with traffic density. It appears that in non-
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PRELIMINARY ORAFT
urban environments, street dust ranges from 80 to 130 Hg/g, whereas urban street dusts range
from 1,000 to 20,000 pg/g. For the purpose of estimating potential human exposure, an average
value of 90 jjg/g in street dust is assumed for baseline exposure and 1500 pg/g in the discuss-
ions of urban environments.
Household dust is also a normal component of the home environment. It accumulates on all
exposed surfaces, especially furniture, rugs, and windowsills. In some households of workers
exposed occupationally to lead dusts, the worker may carry dust home in amounts too small for
efficient removal but containing lead concentrations much higher than normal baseline values.
Host of the dust values for nonurban household environments fall in the range of 50 to
500 MS/g- A value of 300 Mfl/g is assumed. The only natural lead in dust would be some frac-
tion of that derived from soil lead. A value of 10 pg/g seems reasonable, since some of the
soil lead is of atmospheric origin. Children ingest about 5 times as much dust as adults,
most of the excess being street dusts from sidewalks and playgrounds. Exposure to occupation-
al lead by children would be through clothing brought home by parents.
The values derived or assumed in the preceeding sections are summarized on Table 1-8.
These values represent only consumption, not absorption of lead by the human body.
1.7.6 Additional Exposures
There are many conditions, even in nonurban environments, where an Individual may in-
crease his lead exposure by choice, habit, or unavoidable circumstance. These conditions are
discussed as separate exposures to be added as appropriate to the baseline of human exposure
described above. Most of these additive effects clearly derive from air or dust, few from
water or food. Ambient air lead concentrations are typically higher 1n an urban than a rural
environment. This factor alone can contribute significantly to the potential lead exposure of
Americans, through increases in inhaled air and consumed dust. Produce from urban gardens may
also increase the daily consumption of lead. Some environments may not be related only to
urban living, such as houses with Interior lead paint or lead plumbing, residences near
smelters or refineries, or family gardens grown on high-lead soils. Occupational exposures
¦ay also be in an urban or rural setting. These exposures, whether primarily in the occupa-
tional environment or secondarily in the home of the worker, would be in addition to other ex-
posures in an urban location or from the special cases of lead-based paint or plumbing.
Urban atmospheres. The fact that urban atmospheres have more airborne lead than nonurban
contributes not only to lead consumed by inhalation but also to increased amounts of lead in
dust. Typical urban atmospheres contain 0.5-1.0 yg Pb/m3. Other variable are the amount of
indoor filtered air breathed by urban residents, the amount of time spent indoors, and the
amount of time spent on freeways. Dusts vary from 500 to 3000 pg/g in urban environments.
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TABLE 1-8. SUMMARY OF BASELINE HUMAN EXPOSURES TO LEAD
Units are in mg/day
Source
Total
lead
Consumed
Natural
Lead
Consumed
Soil
Indirect
Atmospheric
Lead*
Direct
Atmospheric
Lead*
Lead from
Solder or
Other Metals
Lead of
Undetermined
Origin
Chi Id-2 yr old
Inhaled Air
0.5
0.001
»
0.5
-
-
Food
28.7
0.9
0.9
10.9
10.3
17.6
Water & beverages
11.5
0.01
2.1
1.2
7.8
-
Dust
21.0
0.6
19.0
—_
1,4
Total
61.4
1.5
3.0
31.6
18.1
19.0
Percent
100%
2.4%
4.9%
51.5%
29.5%
22.6%
Adult female
Inhaled air
1.0
0.002
-
1.0
-
-
Food
33.2
1.0
1.0
12.6
11.9
21.6
Water & beverages
17,9
0.01
3.4
2.0
12.5
-
Dust
4.5
0.2
2.9
1.4
Total
56.6
1.2
4.4
18.5
24.4
23.0
Percent
100%
2. IX
7.8%
32.7%
43.1%
26.8%
Adult male
Inhaled air
1.0
0.002
-
1.0
-
-
Food
45.7
1.4
1.4
17.4
16.4
31.5
Water & beverages
25.1
0.1
4.7
2.8
17.5
-
Dust
4.5
0.2
2.9
_
1.4
Total
76.3
1.7
6.1
24.1
33.9
32.9
Percent
100%
2.2%
8.0%
31.6%
44.4%
27.1%
•Indirect atmospheric lead has been previously incorporated into soil, and will probably remain in the soil
for decades or longer. Direct atmospheric lead has been deposited on the surfaces of vegetation and living
areas or incorporated during food processing shortly before human consumption.
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PRELIMINARY DRAFT
Houses with interior lead paint. In 1974, the Consumer Product Safety Commission col-
lected household paint samples and analyzed them for lead content (National Academy of
Sciences, National Research Council, 1976).
Flaking paint can cause elevated lead concentrations in nearby soil. For example, Hardy
et al. (1971) measured soil lead levels of 2000 pg/g next to a barn 1n rural Massachusetts. A
steady decrease in lead level with Increasing distance from the barn was shown, reaching 60
pg/g at fifty feet from the barn. Ter Haar and Arnow (1974) reported elevated soil lead
levels 1n Detroit near eighteen old wood frame houses painted with lead-based paint. The
average soil lead level within two feet of a house was just over 2000 pg/g; the average con-
centration at ten feet was slightly more than 400 pg/g. The same author reported smaller soil
lead elevations in the vicinity of eighteen brick veneer houses in Detroit. Soil lead levels
near painted barns located in rural areas were similar to urban soil lead concentrations near
painted houses, suggesting the importance of leaded paint at both urban and rural locations.
The baseline lead concentration for household dust of 300 pg/g was increased to 2000 pg/g for
houses with interior lead based paints. The additional 1700 pg/g would add 85 pg Pb/day to
the potential exposure of a child. This increase would occur in an urban or nonurban environ-
ment and would be in addition to the urban residential increase if the lead-based painted
house were in an urban environment.
Family gardens. Several studies have shown potentially higher lead exposure through the
consumption of home-grown produce from family gardens grown on high lead soils or near sources
of atmospheric lead. In family gardens, lead may reach the edible portions of vegetables by
deposition of atmospheric lead directly onto aboveground plant parts or onto soil, or by the
flaking of lead-containing paint chips from houses. Air concentrations and particle size dis-
tributions are the important determinants of deposition to soil or vegetation surfaces. Even
at relatively high air concentrations (1.5 pg/m3) and deposition velocity (0.5 cm/sec), it is
unlikely that surface deposition alone can account for more than 2-5 pg/g lead on the surface
of lettuce during a 21-day growing period. It appears that a significant fraction of the lead
1n both leafy and root vegetables derives from the soil.
Houses with lead plumbing. The Glasgow Duplicate Diet Study (United Kingdom Directorate
on Environmental Pollution, 1982) reports that children approximately 13 weeks old living in
lead-plumbed houses consume 6-480 pg Pb/day. Water lead levels 1n the 131 homes studied
ranged from less than 50 to over 500 pg/1. Those children and mothers living in the homes
containing high water lead levels generally had greater total lead consumption and higher
blood lead levels, according to the study. Breast-fed infants were exposed to much less lead
than bottle-fed Infants. The results of the study suggest that Infants living 1n lead-plumbed
homes may have exposure to considerable amounts of lead. This conclusion was also demonstrat-
ed by Sherlock et al. (1982) in a duplicate diet study in Ayr, Scotland.
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Residences near swelters and refineries. Air concentrations within 2 km of lead shelters
and refineries average 5-15 vg/m3. Between Inhaled air and dust, a child in this circumstance
would be exposed to 1300 Mfl Pb/day above background levels. Exposures to adults would be much
less, since they consume only 20 percent of the dusts children consume.
Occupational exposures. The highest and most prolonged exposures to lead are found among
workers in the lead smelting, refining, and manufacturing Industries (World Health Organiza-
tion, 1977). In all work areas, the major route of lead exposure is by inhalation and inges-
tion of lead-bearing dusts and fumes. Airborne dusts settle out of the air onto food, water,
the workers' clothing, and other objects, and may be subsequently transferred to the mouth.
Therefore, good housekeeping and good ventilation have a major impact on exposure. Even tiny
amounts (10 ng) of 100,000 pg/g dust can account for 1,000 pg/day exposure.
The greatest potential for high-level occupational exposure exists in the process of lead
smelting and refining. The most hazardous operations are those in which molten lead and lead
alloys are brought to high temperatures, resulting in the vaporization of lead, because con-
densed lead vapor or fume has, to a substantial degree, a small (resplrable) particle size
range.
When metals that contain lead or are protected with a lead-containing coating are heated
in the process of welding or cutting, copious quantities of lead in the resplrable size range
may be emitted. Under conditions of poor ventilation, electric arc welding of zinc silicate-
coated steel (containing 29 mg Pb/in2 of coating) produces breathing-zone concentrations of
lead reaching 15,000 pg/m3, far in excess of 450 pg/m3, the current occupational short-term
exposure limit in the United States. In a study of salvage workers using oxy-acetylene cut-
ting torches on lead-painted structural steel under conditions of good ventilation, breathing-
zone concentrations of lead averaged 1200 pg/m3 and ranged as high as 2400 pg/m3.
At all stages in battery manufacture except for final assembly and finishing, workers are
exposed to high air lead concentrations, particularly lead oxide dust. Excessive concentra-
tions, as great as 5400 pg/m3, have been quoted by the World Health Organization (1977). The
hazard in plate casting, which is a molten-metal operation, is from the spillage of molten
waste products, resulting in dusty floors.
Workers involved in the manufacture of both tetraethyl lead and tetramethyl lead, two
alkyl lead compounds, are exposed to both inorganic and alky! lead. The major potential
hazard in the manufacture of tetraethyl lead and tetramethyl lead is from skin absorption, but
this is guarded against by the use of protective clothing.
In both the rubber products industry and the plastics industry there are potentially high
exposures to lead. The potential hazard of the use of lead stearate as a stabilizer in the
manufacture of polyvinyl chloride was noted in the 1971 United Kingdom Department of Employ-
ment, Chief Inspector of Factories (1972). The source of this problem is the dust that is
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PRELIMINARY DRAFT
generated when the lead stearate 1s milled and mixed with the polyvinyl chloride and the plas-
ticizer. An encapsulated stabilizer that greatly reduces the occupational hazard is reported
by Fischbein et al. (1982). Sakurai et al. (1974), in a study of bioindicators of lead expo-
sure, found ambient air concentrations averaging 58 pg/m3 in the lead-covering department of a
rubber hose manufacturing plant.
The manufacture of cans with leaded seams may expose workers to elevated environmental
lead levels. Bishop (1980) reports airborne lead concentrations of 25 to 800 pg/m3 in several
can manufacturing plants in the United Kingdom. Between 23 percent and 54 percent of the air-
borne lead was associated with respirable particles. Firing ranges may be characterized by
high airborne lead concentrations, hence instructors who spend considerable amounts of time in
such areas may be exposed to lead. Anderson et al. (1977) discuss plumbism in a 17-year-old
male employee of a New York City firing range, where airborne lead concentrations as great as
1000 pg/m3 were measured during sweeping operations. Removal of leaded paint from walls and
other surfaces in old houses may pose a health hazard. Feldman (1978) reports an airborne
lead concentration of 510 pg/m3, after 22 minutes of sanding an outdoor post coated with paint
containing 2.5 mg Pb/cm2. After only five minutes of sanding an indoor window sill containing
0.8-0.9 mg Pb/cm2, the air contained 550 pg/m3. Garage mechanics may be exposed to excessive
lead concentrations. Clausen and Rastogi (1977) report airborne lead levels of 0.2-35.5 pg/m3
in ten garages in Denmark; the greatest concentration was measured in a paint workshop. Used
motor oils were found to contain 1500-3500 pg Pb/g, while one brand of gear oil, unused, con-
tained 9280 pg Pb/g. The authors state that absorption through damaged skin could be an
important exposure pathway. Other occupations involving risk of lead exposure include stained
glass manufacturing and repair, arts and crafts, and soldering and splicing.
Secondary occupational exposure. The amount of lead contained in pieces of cloth 1 in2
cut from bottoms of trousers worn by lead workers ranged from 700 to 19,000 pg, with a median
of 2,640 pg. In all cases, the trousers were worn under coveralls. Dust samples from 25
households of smelter workers ranged from 120 to 26,000 pg/g, with a median of 2,400 pg/g.
Special habits or activities. The quantity of food consumed per body weight varies
greatly with age and somewhat with sex. A two-year-old child weighing 14 kg eats and drinks
1.5 kg food and water per day. This is 110 g/kg, or 3 times the consumption of an 80 kg adult
male, who eats 39 g/kg.
Children place their mouths on dust collecting surfaces and lick non-food items with
their tongues. This fingersucking and mouthing activity are natural forms of behavior for
young children which expose them to some of the highest concentrations of lead 1n their envi-
ronment. A single gram of dust may contain ten times more lead than the total diet of the
child.
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PRELIMINARY DRAFT
Lead Is also present in tobacco. The World Health Association (1977) estimates a lead
content of 2.5-12.2 jig per cigarette; roughly two to six percent of this lead nay be inhaled
by the smoker. The National Academy of Sciences (1980) has used these data to conclude that a
typical urban resident who smokes 30 cigarettes per day may inhale roughly equal amounts of
lead from smoking and from breathing urban air. The average adult consumption of table wine
in the U.S. is about 12 g. Even at 0.1 which is ten times higher than drinking water,
wine does not appear to represent a significant potential exposure. At one liter/day,
however, lead consumption would be greater than the total baseline consumption. McDonald
(1981) points out that older wines with lead foil caps may represent a hazard, especially if
they have been damaged or corroded. Wai et al. (1979) found the lead content of wine rose
from 200 to 1200 pg/liter when the wine was allowed to pass over the thin ring of residue left
by the corroded lead foil cap. Newer wines (1971 and later) use other means of sealing.
Pica Is the compulsive, habitual consumption of non-food items. In the case of paint
chips and soil, this habit can present a significant lead exposure to the afflicted person.
There are very little data on the amounts of paint or soil eaten by children with varying de-
grees of pica. Exposure can only be expressed on a unit basis. Billick and Gray (1978) re-
port lead concentrations of 1000-5000 MJ/em2 in lead-based paint pigments. A single chip of
paint can represent greater exposure than any other source of lead. A gram of urban soil nay
have 150-2000 yg lead.
Beyond the baseline level of human exposure, additional amounts of lead consumption are
largely a matter of Individual choice or circumstance. Most of these additional exposures a-
rise directly or indirectly from atmospheric lead, and in one or more ways probably affect 90
percent of the American population. In some cases, the additive exposure can be fully quan-
tified and the amount of lead consumed can be added to the baseline consumption. These may be
continuous (urban residence), or seasonal (family gardening) exposures. Some factors can be
quantified on a unit basis because of wide ranges in exposure duration or concentration. For
example, factors affecting occupational exposure are air lead concentrations (10-4000 pg/m3),
use and efficiency of respirators, length of time of exposure, dust control techniques, and
worker training in occupational hygiene.
Ambient airborne lead concentrations showed no marked trend from 1965 to 1977. Over the
past five years, however, distinct decreases occurred. Mean urban air concentration has
3 3
dropped from 0.91 Mg/« 1977 to 0.32 ng/m 1n 1980. These decreases reflect the smaller lead
emissions from mobile sources in recent years. Airborne size distribution data indicate that
most of the airborne lead mass is found in submlcron particles. Atmospheric lead is deposited
on vegetation and soil surfaces, entering the fcuman food chain through contamination of grains
and leafy vegetables, of pasture lands, and of soil moisture taken up by all crops. Lead con-
tamination of drinking water supplies appears to originate mostly from within the distribution
system.
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PRELIMINARY DRAFT
Host people receive the largest portion of their lead Intake through foods. Unprocessed
foods such as fresh fruits and vegetables receive lead by atmospheric deposition as well as
uptake from soil; crops grown near heavily traveled roads generally have greater lead levels
than those grown at greater distances from traffic. For many crops the edible internal por-
tions of the plant (e.g., kernels of corn and wheat) have considerably less lead than the
outer, more exposed parts such as stems, leaves, and husks. Atmospheric lead accounts for
about 30 percent of the total adult lead exposure, and 50 percent of the exposure for chil-
dren. Processed foods have greater lead concentrations than unprocessed foods, due to lead
Inadvertently added during processing. Foods packaged in spidered cans have much greater lead
levels than foods packaged in other types of containers. About 45 percent of the baseline
adult exposure to lead results from the use of solder lead in packaging food and distributing
drinking water.
Significant amounts of lead In drinking water can result from contamination at the water
source and from the use of lead solder 1n the water distribution system. Atmospheric deposi-
tion has been shown to Increase lead 1n rivers, reservoirs, and other sources of drinking
water; in some areas, however, lead pipes pose a more serious problem. Soft, acidic water in
homes with lead plumbing may have excessive lead concentrations. Besides direct consumption
of the water, exposure may occur when vegetables and other foods are cooked 1n water con-
taining lead.
All of the categories of potential lead exposure discussed above may influence or be in-
fluenced by dust and soil. For example, lead in street dust is derived primarily from
vehicular emissions, while leaded house dust may originate from nearby stationary or mobile
sources. Food and water may Include lead adsorbed from soil as well as deposited atmospheric
material. Flaking leadbased paint has been shown to increase soil lead levels. Natural con-
centrations of lead in soil average approximately 15 pg/g; this natural lead, in addition to
anthropogenic lead emissions, influences human exposure.
Americans living 1n rural areas away from sources of atmospheric lead consume 50 to 75 pg
Pb/day from all sources. Circumstances which can increase this exposure are: urban residence
(25 to 100 pg/day), family garden on high lead soil (800 to 2000 pg/day), houses with interior
lead-based paint (20 to 85 pg/day), and residence near a smelter (400 to 1300 pg/day). Occu-
pational settings, smoking and wine consumption also can Increase consumption of lead accord-
ing to the degree of exposure.
A number of manmade materials are known to contain lead, the most important being paint
and plastics. Lead-based paints, although no longer used, are a major problem 1n older homes.
Small children who Ingest paint flakes can receive excessive lead exposure. Incineration of
plastics may emit large amounts of lead Into the atmosphere. Because of the Increasing use of
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PRELIMINARY DRAFT
plastics, this source is likely to become more important. Other marinade materials containing
lead include colored dyes, cosmetic products, candle wicks, and products made of pewter and
silver.
The greatest occupational exposures are found in the lead smelting and refining indus-
tries. Excessive airborne lead concentrations and dust lead levels are occasionally found 1n
primary and secondary smelters; smaller exposures are associated with mining and processing of
the lead ores. Welding and cutting of metal surfaces coated with lead-based paint may also
result in excessive exposure. Other occupations with potentially high exposures to lead in-
clude the manufacture of lead storage batteries, printing equipment, alkyl lead, rubber pro-
ducts, plastics, and cans; individuals removing lead paint from walls and those who work in
indoor firing ranges may also be exposed to lead.
Environmental contamination by lead should be measured in terms of the total amount of
lead emitted to the biosphere. American industry contributes several hundred thousand tons of
lead to the environment each year: 35,000 tons from petroleum additives, 50,000 tons from am-
munition, 45,000 tons in glass and ceramic products, 16,000 tons in paint pigments, 8,000 tons
in food can solder, and untold thousands of tons of captured wastes during smelting, refining,
and coal combustion. These are uses of lead which are generally not recoverable, thus they
represent a permanent contamination of the human or natural environment. Although much of
this lead is confined to municipal and industrial waste dumps, a large amount is emitted to
the atmosphere, waterways, and soil, to become a part of the biosphere.
Potential human exposure can be expressed as the concentrations of lead in those environ-
mental components (air, dust, food, and water) that interface with man. It appears that, with
the exception of extraordinary cases of exposure, about 100 mg of lead are consumed daily by
each American. This amounts to only 8 tons, or less than 0.01 percent of the total environ-
mental contamination.
1.8 EFFECTS OF LEAD ON ECOSYSTEMS
The principle sources of lead entering an ecosystem are: the atmosphere (from automotive
emissions), paint chips, spent ammunition, the application of fertilizers and pesticides, and
the careless disposal of lead-acid batteries or other industrial products. Atmospheric lead
is deposited on the surfaces of vegetation as well as on ground and water surfaces. In ter-
restrial ecosystems, this lead is transferred to the upper layers of the soil surface, where
it may be retained for a period of several years. The movement of lead within ecosystems is
Influenced by the chemical and physical properties of lead and by the biogeochemical pro-
perties of the ecosystem. Lead is non~degradable, but in the appropriate chemical' environ-
ment, may undergo transformations which affect its solubility (e.g., formation of lead sulfate
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PRELIMINARY ORAFT
in soils), its bioavailability (e.g., chelation with humic substances), or its toxicity (e.g.,
chemical methylation). Although the situation is extremely complex, it is reasonable to state
that most plants cannot survive in soil containing 10,000 pg lead/g dry weight if the pH is
below 4.5 and the organic content 1s below 5 percent.
There is wide variation in the mass transfer of lead from the atmosphere to terrestrial
ecosystems. Smith and Siccama (1981) report 270 g/ha-yr in the Hubbard Brook forest of New
Hampshire, Lindberg and Harriss (1981) found 50 g/ha-yr in the Walker Branch watershed of
Tennessee; and Ellas et al. (1976) found 15 g/ha-yr In a remote subalpine ecosystem of
California. Jackson and Watson (1977) found 1,000,000 g/ha-yr near a smelter in southeastern
Missouri. Getz et al. (1979) estimated 240 g/ha-yr by wet precipitation alone in a rural eco-
system largely cultivated, and 770 g/ha-yr in an urban ecosystem.
One factor causing great variation is remoteness from source, which translates to lower
air concentrations, smaller particles, and greater dependence on wind as a mechanism of depo-
sition. Another factor is type of vegetation cover. Deciduous leaves may, by the nature of
their surface and orientation in the wind stream, be more suitable deposition surfaces than
conifer needles.
There are three known conditions under which lead may perturb ecosystem processes (see
Figured 1-12). At soil concentrations of 1000 pg/g or higher, delayed decomposition nay
result from the elimination of a single population of decomposer microorganisms. Secondly, at
concentrations of 500-1000 yg/g, populations of plants, microorganisms, and invertebrates may
shift toward lead tolerant populations of the same or different species. Finally, the normal
biogeochemical process which purifies and repurifies calcium in grazing and decomposer food
chains may be circumvented by the addition of lead to vegetation and animal surfaces. This
third effect can be measured at all ambient atmospheric concentrations of lead.
Some additional effects may occur due to the uneven distribution of lead in ecosystems.
It 1s known that lead accumulates in soil, especially soil with high organic content.
Although no firm documentation exists, it is reasonable to assume from the known chemistry of
lead in soil that: (1) other metals may be displaced from binding sites on the organic
matter; (2) the chemical breakdown of Inorganic soil fragments may be retarded by interference
of lead with the action of fulvic acid on iron bearing crystals; and (3) lead in soil may be
in equilibrium with moisture films surrounding soil particles and thus available for uptake by
plants.
Two principles govern ecosystem functions: (1) energy flows through an ecosystem; and
(2) nutrients cycle within an ecosystem. Energy usually enters the ecosystem in the form of
sunlight and leaves as heat of respiration. Unlike energy, nutrient and non-nutrient elements
are recycled by the ecosystem and transferred from reservoir to reservoir in a pattern usually
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GRAZERS
HERBIVORES
CARNIVORES
CARNIVORES
DECOMPOSERS
DETRITUS
INORGANIC
NUTRIENTS
Figure 1*12. This figure depicts cycling processes within the major components of a
terrestrial ecosystem, i.e. prlmery producers, grazers arid decomposers. Nutrient and
non-nutrient elements are stored in reservoirs within these components. Processes
that take place within reservoirs regulate the flow of elements between reservoirs
along established pathways. The rata of flow is in part a function of the concentra-
tion in the preceding reservoir. Lead accumulates in decomposer reservoirs which
have a high binding capacity for this metal. It is likely that the rata of flow away
from these reservoirs has increased in past decades and will continue to increase for
some time until the decomposer reservoirs are in equilibrium with the entire
ecosystem. Inputs to and outputs from the ecosystem as a whole are not shown.
Source: Adapted from Swift et al. (1979!.
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referred to as a biogeochemical cycle (Brewer, 1979, p. 139). The reservoirs correspond ap-
proximately to the food webs of energy flow. Although elements may enter (e.g., weathering of
soil) or leave the ecosystem (e.g., stream runoff), the greater fraction of the available mass
of the element 1s usually cycled within the ecosystem.
Ecosystems have boundaries. These boundaries may be as distinct as the border of a pond
or as arbitrary as an imaginary circle drawn on a map. Many trace metal studies are conducted
in watersheds where some of the boundaries are determined by topography. For atmospheric in-
puts to terrestrial ecosystems, the boundary is usually defined as the surface of vegetation,
exposed rock or soil. Non-nutrient elements differ little from nutrient elements in their
biogeochenlcal cycles. Quite often, the cycling patterns are similar to those of a major
nutrient. In the case of lead, the reservoirs and pathways are very similar to those of
calcium.
Naturally occurring lead from the earth's crust is commonly found in soils and the atmos-
phere, Lead may enter an ecosystem by weathering of parent rock or by deposition of atmos-
pheric particles. This lead becomes a part of the nutrient medium of plants and the diet of
animals. All ecosystems receive lead from the atmosphere.
In prehistoric times, the contribution of lead from weathering of soil was probably about
4g Pb/ha-yr and from atmospheric deposition about 0.02 g Pb/ha-yr. Weathering rates are pre-
sumed to have remained the same, but atmospheric inputs are believed to have increased to
180 g/ha-yr in natural and some cultivated ecosystems, and 3000 g/ha*yr in urban ecosystems
and along roadways. In every terrestrial ecosystem of the Northern Hemisphere, atmospheric
lead deposition now exceeds weathering by a factor of at least 10, sometimes by as much as
1000.
Many of the effects of lead on plants, microorganisms, and ecosystems arise from the fact
that lead from atmospheric and weathering inputs is retained by soil. Geochemical studies
show that less than 3 percent of the inputs to a watershed leave by stream runoff. Lead in
natural soils now accumulates on the surface at an annual rate of 5-10 percent of the natural
lead. One effect of cultivation is that atmospheric lead is mixed to a greater depth than the
0-3 cm of natural soils.
Most of the effects on grazing vertebrates stem from the deposition of atmospheric par-
ticles on vegetation surfaces. Atmospheric deposition nay occur by either of two mechanisms.
Wet deposition (precipitation scavenging through ralnout or washout) generally transfers lead
directly to the soil. Dry deposition transfers particles to all exposed surfaces. Large par-
ticles (>4 pm) are transferred by gravitational mechanisms, small particles (<0,5 (j») are also
deposited by wind-related mechanisms.
If the air concentration is known, ecosystem inputs from the atmosphere can be predicted
over time and under normal conditions. These Inputs and those from the weathering of soil
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determine the concentration of lead In the nutrient media of plants, animals, and micro-
organisms. It follows that the concentration of lead in the nutrient medium determines the
concentration of lead In the organism and this in turn determines the effects of lead on the
organism. The fundamental nutrient medium of a terrestrial ecosystem is the soil moisture
film which surrounds organic and Inorganic soil particles. This film of water is in equi-
librium with other soil components and provides dissolved inorganic nutrients to plants.
Studies have shown the lead content of leafy vegetation to be 90 percent anthropogenic,
even in remote areas (Crump and Barlow, 1980; Elias et al., 1976, 1978). The natural lead
content of nuts and fruits may be somewhat higher than leafy vegetation, based on internal
lead concentrations of modern samples (Elias et al. 1982).
Because lead 1n soil 1s the source of most effects on plants, microorganisms, and eco-
systems, it is important to understand the processes that control the accumulation of lead in
soil. Major components of soil are: (1) fragments of inorganic parent rock material;
(2) secondary inorganic minerals; (3) organic constituents, primarily humic substances, which
are residues of decomposition or products of decomposer organisms; (4) Fe-Mn oxide films,
which coat the surfaces of all soil particles and have a high binding capacity for metals;
(5) soil microorganisms, most commonly bacteria and fungi, although protozoa and soil algae may
also be found; and (6) soil moisture, the thin film of water surrounding soil particles which
is the nutrient medium of plants.
The concentration of lead ranges from 5 to 30 pg/g in the top 5 cm of most soils not
adjacent to sources of industrial lead, although 5 percent of the soils contain as much as
800 pg/g. Aside from surface deposition of atmospheric particles, plants in North America
average about 0.5-1 pg/g dw (Peterson, 1978) and animals roughly 2 pg/g (Forbes and Sanderson,
1978). Thus, soils contain the greater part of total ecosystem lead. In soils, lead in
parent rock fragments is tightly bound within the crystalline structures of the inorganic soil
minerals. It is released to the ecosystem only by surface contact with soil moisture films.
Hutchinson (1980) has reviewed the effects of acid precipitation on the ability of soils
to retain cations. Excess calcium and other metals are leached from the A horizon of soils by
rain with a pH more acidic than 4.5. Most soils in the eastern United States are normally
acidic (pH 3.5-5.2) and the leaching process is a part of the complex equilibrium maintained
in the soil system. By increasing the leaching rate, acid rain can reduce the availability of
nutrient metals to organisms dependent on the top layer of soil. It appears that acidifica-
tion of soil may increase the rate of removal of lead from the soil, but not before several
major nutrients are removed first. The effect of acid rain on the retention of lead by soil
moisture is not known.
Atmospheric lead may enter aquatic ecosystems by wet or dry deposition or by the
erosional transport of soil particles. In waters not polluted by industrial, agricultural, or
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¦unlclpal effluents, the lead concentration is usually less than 1 pg/1. Of this amount,
approximately 0.02 |jg/1 is natural lead and the rest is anthropogenic lead, probably of atmos-
pheric origin (Patterson, 1980). Surface waters mixed with urban effluents may frequently
reach lead concentrations of 50|jg/1> and occasionally higher. In still water, lead is
removed from the water column by the settling of lead-containing particulate matter, by the
formation of insoluble complexes, or by the adsorption of lead onto suspended organic
particles. The rate of sedimentation is determined by temperature, pH, oxidation-reduction
potential, ionic competition, the chemical form of lead in water, and certain biological acti-
vities (Jenne and Luoma, 1977). McNurney et al. (1977) found 14 pg Pb/g in stream sediments
draining cultivated areas and 400 pg/g in sediments associated with urban ecosystems.
1.8.1 Effects on Plants
Some physiological and biochemical effects of lead on vascular plants have been detected
under laboratory conditions at concentrations higher than normally found in the environment.
The commonly reported effects are the Inhibition of photosynthesis, respiration or cell elon-
gation, all of which reduce the growth of the plant (Koeppe, 1981). Lead may also induce pre-
mature senescence, which may affect the long-term survival of the plant or the ecological suc-
cess of the plant population. Most of the lead 1n or on a plant occurs on the surfaces of
leaves and the trunk or stem. The surface concentration of lead in trees, shrubs, and grasses
exceeds the internal concentration by a factor of at least five (El 1 as et al, 1978). There is
little or no evidence of lead uptake through leaves or bark. Foliar uptake, 1f it does occur,
cannot account for more than 1 percent of the uptake by roots, and passage of lead through
bark tissue has not been detected (Arvik and Zimdahl, 1974; reviewed by Koeppe, 1981; Zimdahl,
1976). The major effect of surface lead at ambient concentrations seems to be on subsequent
components of the grazing food chain and on the decomposer food chain following Utterfall
(Ellas et al., 1982).
Uptake by roots 1s the only major pathway for lead Into plants. The amount of lead that
enters plants by this route is determined by the availability of lead 1n soil, with apparent
variations according to plant species. Soil cation exchange capacity, a major factor, 1s de-
termined by the relative size of the clay and organic fractions, soil pH, and the amount of
Fe-Mn oxide films present (NHagu, 1978). Of these, organic humus and high soil pH are the
dominant factors In Immobilizing lead. Under natural conditions, most of the total lead 1n
soil would be tightly bound within the crystalline structure of inorganic soil fragments, un-
available to soil moisture. Available lead, bound on clays, organic colloids, and Fe-Mn
films, would be controlled by the slow release of bound lead from Inorganic rock sources. Be-
cause lead 1s strongly Immobilized by humlc substances, only a small fraction (perhaps 0.01 -
percent 1n soils with 20 percent organic matter, pH 5.5) 1s released to soil moisture.
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Two defensive mechanims appear to exist in the roots of plants for removing lead fro* the
stream of nutrients flowing to the above-ground portions of plants. Lead may be deposited
with cell wall material exterior to the individual root cells, or may be sequestered in organ-
elles within the root cells. Any lead not captured by these mechanisms would likely move with
nutrient metals cell-to-cell through the symplast and into the vascular system. Uptake of
lead by plants may be enhanced by symbiotic associations with mycorrhizal fungi. The three
primary factors that control the uptake of nutrients by plants are the surface area of the
roots, the ability of the root to absorb particular ions, and the transfer of ions through the
soil. The symbiotic relationship between mycorrhizal fungi and the roots of higher plants can
increase the uptake of nutrients by enhancing all three of these factors.
The translocation of lead to aboveground portions of the plant is not clearly understood.
Lead may follow the same pathway and be subject to the same controls as a nutrient metal such
as calcium. There may be several mechanisms that prevent the translocation of lead to other
plant parts. The primary mechanisms may be storage in cell organelles or adsorption on cell
walls. Some lead passes into the vascular tissue, along with water and dissolved nutrients,
and is carried to physiologically active tissue of the plant. Evidence that lead in contami-
nated soils can enter the vascular system of plants and be transported to aboveground parts
may be found in the analysis of tree rings. These chronological records confirm that lead can
be translocated in proportion to the concentrations of lead in soil.
Because most of the physiologically active tissue of plants is involved in growth, main-
tenance, and photosynthesis, 1t is expected that lead might interfere with one or more of
these processes. Indeed, such interferences have been observed in laboratory experiments at
lead concentrations greater than those normally found in the field, except near smelters or
mines (Koeppe, 1981). Inhibition of photosynthesis by lead may be by direct interference with
the light reaction or the indirect interference with carbohydrate synthesis. Miles et al.
(1972) demonstrated substantial inhibition of photosystem II near the site of water splitting,
a biochemical process believed to require manganese. Devi Prasad and Devi Prasad (1982) found
10 percent inhibition of pigment production in three species of green algae at 1 pg/fl, in-
creasing to 50 percent Inhibition at 3 pg/g. Bazzaz et al. (1974, 1975) observed reduced net
photosynthesis which may have been caused indirectly by Inhibition of carbohydrate synthesis.
The stunting of plant growth may be by the inhibition of the growth hormone IAA (indole-
3-ylacetic acid). Lane et al. (1978) found a 25 percent reduction in elongation at 10 pg/g
lead as lead nitrate in the nutrient medium of wheat coleoptiles. Lead may also interfere
with plant growth by reducing respiration or inhibiting cell division. Miller and Koeppe
(1971) and Miller et al. (1975) showed succinate oxidation inhibition in Isolated mitochondria
as well as stimulation of exogenous NADH oxidation with related mitochondrial swelling.
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Nassett et al. (1976), Koeppe (1977), and Malone et al. (1978) described significant inhibi-
tion of lateral root initiation in corn. The interaction of lead with calcium has been shown
by several authors, most recently by Garland and Wilkins (1981), who demonstrated that barley
seedlings (Hordeum vulgare). which were growth inhibited at 2 pg Pb/g sol. with no added
calcium, grew at about half the control rate with 17 Mi Ca/g sol. This relation persisted up
to 25 pg Pb/g sol, and 500 pg Ca/g sol.
These studies of the physiological effects of lead on plants all show some effect at con-
centrations from 2 to 10 pg/g in the nutrient medium of hydroponically-grown agricultural
plants. It is certain that no effects would have been observed at these concentrations had
the lead solutions been added to normal soil, where the lead would have been bound by humic
substances. There is no firm relationship between soil lead and soil moisture lead, because
each soil type has a unique capacity to retain lead and to release that lead to the soil
moisture film surrounding the soil particle. Once in soil moisture, lead seems to pass freely
to the plant root according to the capacity of the plant root to absorb water and dissolved
substances.
It seems reasonable that there may be a direct correlation between lead in hydroponic
media and lead in soil moisture. Hydroponic media typically have an excess of essential
nutrients, including calcium and phosphorus, so that movement of lead from hydroponic media to
plant root would be equal to or slower than movement from soil moisture to plant root.
Even .under the best of conditions where soil has the highest capacity to retain lead,
most plants would experience reduced growth rate (inhibition of photosynthesis, respiration,
or cell elongation) in soils containing 10,000 pg Pb/g or greater. Concentrations approaching
this value typically occur around smelters and near major highways. These conclusions pertain
to soil with the ideal composition and pH to retain the maximum amount of lead. Acid soils or
soils lacking organic matter would inhibit plants at much lower lead concentrations.
The rate at which atmospheric lead accumulates in soil varies from 1.1 mg/m2*yr average
global deposition to 3000 mg/m2«yr near a smelter. Assuming an average density of 1.5 g/cm3,
undisturbed soil to a depth of 2 cm (20,000 cm3/m2) would incur an increase in lead concen-
tration at a rate of 0.04 to 100 ms/Q soil -yr. This means remote or rural area soils may
never reach the 10,000 pg/g threshold but that undisturbed soils closer to major sources may
be within range in the next 50 years.
Some plant species have developed populations tolerant to high lead soils. Using popu-
lations taken from mine waste and uncontaminated control areas, some authors have quantified
the degree of tolerance of Agrostis tenuis (Karataglis, 1982) and Festuca rubra (Wong, 1982)
under controlled laboratory conditions. Root elongation was used as the index of tolerance.
At 36 pg Pb/g nutrient solution, all populations of A. tenuis were completely inhibited. At
12 pg Pb/g, the control populations from low lead soils were completely inhibited, but the
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populations from mine soils achieved 30 percent of their normal growth (growth at no lead in
nutrient solution). At 6 pg/g, the control populations achieved 10 percent of their normal
growth, tolerant populations achieved 42 percent. There were no measurements below 6 pg/g.
These studies support the conclusion that Inhibition of plant growth begins at a lead concen-
tration of less than 1 pg/g soil moisture and becomes completely inhibitory at a level between
3 and 10 pg/g. Plant populations that are genetically adapted to high lead soils may achieve
50 percent of their normal root growth at lead concentrations above 3 pg/g.
When soil conditions allow lead concentrations in soil moisture to exceed 2-10 pg/g, most
plants experience reduced growth due to the inhibition of one or more physiological processes.
Excess calcium or phosphorus may reverse the effect. Plants that absorb nutrients from deeper
soil layers may receive less lead. Acid rain is not likely to release more lead until after
major nutrients have been depleted from the soil. A few species of plants have the genetic
capability to adapt to high lead soils.
Tyler (1972) explained three ways in which lead might interfere with the normal decompo-
sition processes in a terrestrial ecosystem. Lead may be toxic to specific groups of decom-
posers, it may deactivate enzymes excreted by decomposers to break down organic matter, or it
may bind with the organic matter to render it resistant to the action of decomposers. Because
lead in litter may selectively inhibit decomposition by soil bacteria at 2000-5000 pg/g,
forest floor nutrient cycling processes may be seriously disturbed near lead smelters. This
is especially important because approximately 70 percent of plant biomass enters the de-
composer food chain. If decomposition of the biomass is Inhibited, then much of the energy
and nutrients remain unavailable to subsequent components of the food chain. There is also
the possibility that the ability of soil to retain lead would be reduced, as humic substances
are byproducts of bacterial decomposition. Because they are Interdependent, the absence of
one decomposer group in the decomposition food chain seriously affects the success of sub-
sequent groups, as well as the rate at which plant tissue decomposes. Each group may be
affected in a different way and at different lead concentrations. Lead concentrations toxic
to decomposer microbes may be as low as 1 to 5 pg/g or as high as 5000 pg/g. Under conditions
of mild contamination, the loss of one sensitive bacterial population may result in its
replacement by a more lead-tolerant strain. Delayed decomposition has been reported near
smelters, mine waste dumps, and roadsides. This delay 1s generally in the breakdown of litter
from the first stage (0j) to the second (0,,), with intact plant leaves and twigs accumulating
at the soil surface. The substrate concentrations at which lead inhibits decomposition appear
to be very low.
The conversion of ammonia to nitrate in soil is a two-step process mediated by two genera
of bacteria, Nitrosomonas and Nltrobacter. Nitrate is required by all plants, although some
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Maintain a symbiotic relationship with nitrogen-fixing bacteria as an alternate source Of ni-
trogen. Those which do not would be affected by a loss of free-living nitrifying bacteria,
and 1t is known that many trace metals inhibit this nitrifying process. Lead is the least of
these, Inhibiting nitrification 14 percent at concentrations of 1000 msAj soil. Even a 14
percent inhibition of nitrification can reduce the potential success of a plant population, as
nitrate is usually the limiting nutrient In terrestrial ecosystems.
It appears that microorganisms are more sensitive than plants to soil lead pollution and
that changes in the composition of bacterial populations may be an early indication of lead
effects. Delayed decomposition may occur at 750 ^ig Pb/g soil and nitrification inhibition at
1000 mq/9-
1.8.2 Effects on Animals
Forbes and Sanderson (1978) have reviewed reports of lead toxicity 1n domestic and wild
animals, lethal toxicity can usually be traced to consumption of lead battery casings, lead-
based paints, oil wastes, putty, linoleum, pesticides, lead shot, or forage near smelters.
Awareness of the routes of uptake is Important in interpreting the exposure and accumulation
in vertebrates. Inhalation rarely accounts for more than 10 to 15 percent of the daily intake
of lead (National Academy of Sciences, 1980). Food is the largest contributor of lead to ani-
mals. The type of food an herbivore eats determines the rate of lead ingestion. Wore than 90
percent of the total lead 1n leaves and bark may be surface deposition, but relatively little
surface deposition may be found on some fruits, berries, and seeds which have short exposure
times. Roots Intrinsically have no surface deposition. Similarly, ingestion of lead by a
carnivore depends mostly on deposition on herbivore fur and somewhat less on lead in herbivore
tissue.
The type of food eaten is a major determinant of lead body burdens in small mammals.
Goldsmith and Scanlon (1977) and Scanlon (1979) measured higher lead concentrations in insec-
tivorous species than in herbivorous, confirming the earlier work of Quarles et al. (1974)
which showed body burdens of granlvores
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PRELIMINARY DRAFT
Hematological and neurological responses are the most commonly reported effects of
extended lead exposures In aquatic vertebrates. Hematological effects include the disabling
and destruction of mature red blood cells and the inhibition of the enzyme ALA-D required for
hemoglobin synthesis. At low exposures, fish compensate by forming additional red blood
cells. These red blood cells often do not reach maturity. At higher exposures, the fish
become anemic. Symptoms of neurological responses are difficult to detect at low exposure,
but higher exposure can induce neuromuscular distortion, anorexia, and muscle tremors. Spinal
curvature eventually occurs with time or increased concentration.
Insects have lead concentrations that correspond to those found in their habitat and
diet. Herbivorous invertebrates have lower concentrations than do predatory types. Among the
herbivorous groups, sucking insects have lower lead concentrations than chewing insects,
especially in regions near roadsides, where more lead is found on vegetation surfaces.
Williamson and Evans (1972) found that gradients away from roadsides are not the same as with
vertebrates, in that invertebrate lead decreases more slowly than vertebrate lead relative to
decreases in soil lead. In Cepaea hortensis. a terrestrial snail, Williamson (1979) found
most of the lead in the digestive gland and gonadal tissue. A continuation of the study
(Williamson, 1980) showed that body weight, age, and daylength influenced the lead concentra-
tions in soft tissues. Beeby and Eaves (1983) addressed the question of whether uptake of
lead in the garden snail, Helix aspersa, is related to the nutrient requirement for calcium
during shell formation and reproductive activity. They found both metals were strongly cor-
related with changes in dry weight and little evidence for correlation of lead with calcium
independent of weight gain or loss.
Gish and Christensen (1973) found lead in whole earthworms to be correlated with soil
lead, with little rejection of lead by earthworms. Consequently, animals feeding on earth-
worms from high lead soils might receive toxic amounts of lead in their diets, although there
was no evidence of toxic effects on the earthworms. Ash and Lee (1980) cleared the digestive
tracts of earthworms and still found direct correlation of lead in earthworms with soil lead;
in this case, soil lead was inferred from fecal analyses. Ireland and Richards (1977) also
found some localization of lead in subcellular organelles of chloragogue and intestinal
tissue. In view of the fact that chloragocytes are believed to be involved with waste storage
and glycogen synthesis, the authors concluded that this tissue is used to sequester lead in
the manner of vertebrate livers.
Borgmann et al. (1978) found increased mortality in a freshwater snail, Lvmnaea palutris,
associated with stream water with a lead content as low as 19 pg/1. Full life cycles were
studied to estimate population productivity. Although individual growth rates were not
affected, increased mortality! especially at the egg hatching stage, effectively reduced total
blomass production at the population level. Production was 50 percent at 36 yg/1 and 0 per-
cent at 48 MS Pb/1.
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While 1t 1s impossible to establish a safe limit of daily lead consumption, it is reason-
able to generalize that a regular diet of 2 to 8 ng Pb/kg-day body weight over an extended
period of time (Botts, 1977) will cause death in most animals. Animals of the grazing food
Chain are affected most directly by the accumulation of aerosol particles on vegetation sur-
faces, and somewhat indirectly by the uptake of lead through plant roots. Many of fJiese
animals consume more than 1 mg Pb/kg-day in habitats near smelters and roadsides, but no toxic
effects have been documented. Animals of the decomposer food chain are affected indirectly by
lead in soil which can eliminate populations of microorganisms preceeding animals in the food
chain or occupying the digestive tract of animals and aiding in the breakdown of organic mat-
ter. Invertebrates may also accumultate lead at levels toxic to their predators.
Aquatic animals are affected by lead at water concentrations lower than previously con-
sidered safe (50 MS Pb/1) for wildlife. These concentrations occur commonly, but the contri-
bution of atmospheric lead to specific sites of high aquatic lead is not clear.
1.8.3 Effects on Microoganisms
Recent studies have shown three areas of concern where the effects of lead on ecosystems
may be extremely sensitive. First, decomposition is delayed by lead, as some decomposer
microorganisms and invertebrates are inhibited by soil lead. Secondly, the natural processes
of calcium biopurification are circumvented by the accumulation of lead on the surfaces of
vegetation and in the soil reservoir. Thirdly, some ecosystems experience subtle shifts
toward lead tolerant plant populations. These problems all arise because lead in ecosystems
is deposited on vegetation surfaces, accumulates in the soil reservoir, and is not removed
with the surface and ground water passing out of the ecosystem.
Terrestrial ecosystems, especially forests, accumulate a tremendous amount of cellulose
as woody tissue of trees. Few animals can digest cellulose and most of these require
symbiotic associations with specialized bacteria. It is no surprise then, that most of this
cellulose must eventually pass through the decomposer food chain. Because 80 percent or more
of net primary production passes through the decomposing food chain, the energy of this litter
is vital to the rest of the plant community and the inorganic nutrients are vital to plants.
The amount of lead that causes litter to be resistant to decomposition 1s not known.
Doelman and Haanstra (1979a) demonstrated the effects of son lead content on delayed decom-
position: sandy soils lacking organic complexing compounds showed a 30 percent Inhibition of
decomposition at 750 \ig/g, including the complete loss of major bacterial species, whereas the
effect was reduced in clay soils and non-existent In peat soils. Organic matter maintains the
cation exchange capacity of soils. A reduction in decomposition rate was observed by Doelman
and Haanstra (1979a) even at the lowest experimental concentration of lead, leading to the
conclusion that some effect might have occurred at even lower concentrations.
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1.8.4 Effects on Ecosystems
When decomposition is delayed, nutrients may be Uniting to plants. In tropical regions
or areas with sandy soils, rapid turnover of nutrients is essential for the success of the
forest community, Even in a mixed deciduous forest, a significant portion of the nutrients,
especially nitrogen and sulfur, may be found in the litter reservoir (Likens et al. 1977).
Annual litter inputs of calcium and nitrogen to the soil account for about 60 percent of root
uptake. With delayed decomposition, plants must rely on precipitation and soil weathering for
the bulk of their nutrients. Furthermore, the organic content of soil may decrease, reducing
the cation exchange capacity of soil.
Biopurification is a process that regulates the relative concentrations of nutrient to
non-nutrient elements in biological components of a food chain. In the absence of absolute
knowledge of natural lead concentrations, biopurification can be a convenient method for esti-
mating the degree of contamination. It is now believed that members of grazing and decomposer
food chains are contaminated by factors of 30-500, i.e., that 97-99.9 percent of the lead in
organisms is of anthropogenic origin. Burnett and Patterson (1980) have shown a similar pat-
tern for a marine food chain.
It has been observed that plant communities near smelter sites are composed mostly of
lead tolerant plant populations. In some cases, these populations appear to have adapted to
high lead soils, since populations of the same species from low lead soils often do not thrive
on high lead soils. In some situations, it is clear that soil lead concentration has become
the dominant factor in determining the success of plant populations and the stability of the
ecological community.
Inputs of natural lead to ecosystems, approximately 90 percent from rock weathering and
10 percent from atmospheric sources, account for slightly more than the hydro!ogle lead out-
puts in most watersheds. The difference is small and accumulation in the ecosystem is sig-
nificant only over a period of several thousand years. In modern ecosystems, with atmospheric
inputs exceeding weathering by factors of 10-1000, greater accumulation occurs in soils and
this reservoir must be treated as lacking a steady state condition. Qdum and Drifmeyer (1978)
describe the role of detrital particles in retaining a wide variety of pollutant substances,
and this role may be extended to include non-nutrient substances.
It appears that plant communities have a built-in mechanism for purifying their own
nutrient medium. As a plant community matures through successlonal stages, the soil profile
develops a stratified arrangement which retains a layer of organic material near the surface.
This organic layer becomes a natural site for the accumulation of lead and other non-nutrient
metals which might otherwise interfere with the uptake and utilization of nutrient metals.
But the rate of accumulation of lead in this reservoir may eventually exceed the capacity of
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the reservoir. Johnson et al. (1982a) have established a baseline of 80 stations in forests
of the northeast United States. In the Utter component of the forest floor, they measured an
average lead concentration of 150 pg/g- Near a smelter, they measured 700 pg/g and near a
highway, 440 pg/g. They presented some evidence from buried litter that predevelopment con-
centrations were 24 \ig/g.
Lead in the detrital reservoir is determined by the continued input of atmospheric lead
from the litter layer, the passage of detritus through the decomposer food chain, and the rate
of leaching into soil moisture. There is strong evidence that soil has a finite capacity to
retain lead. Harrison et al. (1981) observed that most of the lead in roadside soils above
200 pg/g is found on Fe-Mn oxide films or as soluble lead carbonate. Lead is removed from the
detrital reservoir by the digestion of organic particles in the detrital food chain and by the
release of lead to soil moisture. Both mechanisms result in a redistribution of lead among
all of the reservoirs of the ecosystem at a very slow rate.
Fulvic acid plays an important role in the development of the soil profile. This organic
acid has the ability to remove iron from the lattice structures of inorganic minerals, result-
ing in the decomposition of these minerals as a part of the weathering process. This break-
down releases nutrients for uptake by plant roots. If all binding sites on fulvic acid are
occupied by lead, the role of fulvic acid in providing nutrients to plants will be circum-
vented. While it 1s reasonably certain that such a process is possible, there is no informa-
tion about the soil lead concentrations that would cause such an effect.
Ecosystem inputs of lead by the atmospheric route have established new pathways and
widened old ones. Insignificant amounts of lead are removed by surface runoff or ground water
seepage. It 1s likely that the ultimate fate of atmospheric lead will be a gradual elevation
in lead concentration of all reservoirs in the system, with most of the lead accumulating In
the detrital reservoir.
Because there is no protection from industrial lead once it enters the atmosphere, it is
Important to fully understand the effects of Industrial lead emissions. Of the 450,000 tons
emitted annually on a global basis, 115,000 tons of lead fall on terrestrial ecosystems.
Evenly distributed, this would amount to 0.1 g/ha-yr, which is much lower than the range of 15
to 1,000,000 g/ha-yr reported in ecosystem studies in the United States. Lead has permeated
these ecosystems and accumulated in the soil reservoir where it will remain for decades. With-
in 20 meters of every major highway, up to 10,000 pg Pb have been added to each gram of sur-
face soil since 1930 (Getz et al., 1979). Near smelters, mines, and in urban areas, as much
as 130,000 pg/g have been observed in the upper 2.5 cm of soil (Jennett et al., 1977). At
increasing distances up to 5 kilometers away from sources, the gradient of lead added since
1930 drops to less than 10 pg/g (Page and Ganje, 1970), and 1 to 5 pg/g have been added in
regions more distant than 5 kilometers (Nrlagu, 1978). In undisturbed ecosystems, atmospheric
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lead Is retained by soil organic matter in the upper layer of soil surface. In cultivated
soils, this lead is mixed with soil to a depth of 25 cm.
Because of the special nature of the soil reservoir, it must not be regarded as an infi-
nite sink for lead. On the contrary, atmospheric lead which is already bound to soil will
continue to pass into the grazing and detrital food chains until equilibrium is reached,
whereupon the lead in all reservoirs will be elevated proportionately higher than natural
background levels. This conclusion applies also to cultivated soils, where lead bound within
the upper 25 cm is still within the root zone.
Few plants can survive at soil concentrations 1n excess of 10,000 pg/g, even under opti-
mum conditions. Some key populations of soil microorganisms and invertebrates die off at 1000
ng/g. Herbivores, in addition to a normal diet from plant tissues, receive lead from the sur-
faces of vegetation in amounts that may be 10 times greater than from internal plant tissue.
A diet of 2 to 8 mg/daykg body weight seems to initiate physiological dysfunction in many
vertebrates.
1.8.5 Summary
Some of the known effects, which are documented in detail in the appropriate sections,
are summarized here:
(1) Plants. The basic effect of lead on plants is to stunt growth. This may be through a
reduction of photosynthetic rate, inhibition of respiration, cell elongation, or root develop-
ment, or premature senescence. Some genetic effects have been reported. All of these effects
have been observed in isolated cells or in hydroponically-grown plants in solutions comparable
to 1-2 mg lead/g soil moisture. These concentrations are well above those normally found in
any ecosystem except near smelters or roadsides. Terrestrial plants take up lead from the
soil moisture and most of this lead is retained by the roots. There is no evidence for foliar
uptake of lead and little evidence that lead can be translocated freely to the upper portions
of the plant. Soil applications of calcium and phosphorus may reduce the uptake of lead by
roots.
(2) Animals. Lead affects the central nervous system of animals and their ability to synthe-
size red blood cells. Blood concentrations above 0.4 »g/g (40 MS/dl) can cause observable
clinical symptoms in domestic animals. Calcium and phosphorus can reduce the intestinal
absorption of lead.
(3) Microorganisms. There 1s evidence that lead at environmental concentrations occasionally
found near roadsides and smelters (10,000-40,000 mg/g dw) can eliminate populations of bac-
teria and fungi on leaf surfaces and in soil. Many of those microorganisms play key roles 1n
the decomposition food chain. It is likely that the microbial populations are replaced by
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others of the sane or different species, perhaps less efficient at decomposing organic matter.
There is also evidence that microorganisms can mobilize lead by making it more pheric parti-
cles. This lead becomes a part of the nutrient medium of plants and the diet of animals. All
ecosystems receive lead from the atmosphere.
Perhaps the most subtle effect of lead is on ecosystems. The normal flow of energy
through the decomposer food chain may be interrupted, the composition of communities may shift
toward more lead-tolerant populations, and new biogeochemical pathways may be opened, as lead
flows into and throughout the ecosystem. The ability of an ecosystem to compensate for atmos-
pheric lead inputs, especially in the presence of other pollutants such as acid precipita-
tion, depends not so much on factors of ecosystem recovery, but on undiscovered factors of ec-
osystem stability. Recovery implies that inputs of the perturbing pollutant have ceased and
that the pollutant is being removed from the ecosystem. In case of lead, the pollutant is not
being eliminated from the system nor are the inputs ceasing. Terrestrial ecosystems will
never return to their original, pristine levels of lead concentrations.
1.9 QUANTITATIVE EVALUATION OF LEAD AND BIOCHEMICAL INDICES OF LEAD EXPOSURE IN PHYSIOLOGICAL
MEDIA
The sine qua non of a complete understanding of a toxic agent's effects on an organism,
e.g., dose-effect relationships, is quantitative measurement of either that agent in some bio-
logical medium or a physiological parameter associated with exposure to the agent. Quantita-
tive analysis involves a number of discrete steps, all of which contribute to the overall re-
liability of the final analytical result: sample collection and shipment, laboratory han-
dling, instrumental analysis, and criteria for internal and external quality control.
From a historical perspective, it is clear that the definition of "satisfactory analyt-
ical method" for lead has been steadily changing as new and more sophisticated equipment be-
comes available and understanding of the hazards of pervasive contamination along the analyti-
cal course increases. The best example of this is the use of the definitive method for lead
analysis, isotope-dilution mass spectrometry In tandem with "ultra-clean" facilities and sam-
pling methods, to demonstrate conclusively not only the true extent of anthropogenic input of
lead to the environment over the years but also the relative limitations of most of the meth-
ods for lead measurement used today.
1.9.1 Determinations of Lead in Biological Media
The low levels of lead in biological media, even 1n the face of excessive exposure, and
the fact that sampling of such media must be done against a backdrop of pervasive lead contam-
ination, necessitates that samples be carefully collected and handled. Blood lead sampling is
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best done by venous puncture and collection Into low-lead tubes after careful cleaning of the
puncture site. The use of finger puncture as an alternative method of sampling should be
avoided, if feasible, given the risk of contamination associated with the practice in indus-
trialized areas. While collection of blood onto filter paper enjoyed some popularity in the
past, paper deposition of blood requires special correction for hematrocrit/hemoglobin level.
Urine sample collection requires the use of lead-free containers as well as addition of a
bacteriocide. If feasible, 24-hour sampling is preferred to spot collection. Deciduous teeth
vary in lead content both within and across type of dentition. Thus a specific tooth type
should be uniformly obtained for all study subjects and, if possible, more than a single sam-
ple should be obtained from each subject.
Measurements of lead in blood. Many reports over the years have purported to offer sat-
isfactory analysis of lead in blood and other biological media, often with severe inherent
limitations on accuracy and precision, meager adherence to criteria for accuracy and preci-
sion, and a limited utility across a spectrum of analytical applications. Therefore, it is
only useful to discuss "definitive" and, comparatively speaking, "reference" methods presently
used.
In the case of lead in biological media, the definitive method is isotope-dilution mass
spectrometry (IDMS). The accuracy and unique precision of IDMS arise from the fact that all
manipulations are on a weight basis involving simple procedures, and measurements entail only
lead isotope ratios and not the absolute determinations of the isotopes involved, greatly re-
ducing instrumental corrections and errors. Reproducible results to a precision of one part
4 5
in 10 -10 are routine with appropriately designed and competently operated instrumentation.
Although this methodology is still not recognized in many laboratories, it was the first
breakthrough, in tandem with "ultra-clean" procedures and facilities, to definitive methods
for indexing the progressive increase in lead contamination of the environment over the centu-
ries. Given the expense, required level of operator expertise, and time and effort involved
for measurements by IDMS, this methodology mainly serves for analyses that either require
extreme accuracy and precision, e.g., geochronometry, or for the establishment of analytical
reference material for general testing purposes or the validation of other methodologies.
While the term "reference method" for lead in biological media cannot be rigorously ap-
plied to any procedures in popular use, the technique of atomic absorption spectrometry in its
various configurations or the electrochemical method, anodic stripping voltammetry, come clos-
est to meriting the designation. Other methods that are generally applied in metal analyses
are either limited in sensitivity or are not feasible for use on theoretical grounds for lead
analysis.
Atomic absorption spectrometry (AAS) as applied to analysis of whole blood generally in-
volves flame or flameless micromethods. One macromethod, the Nessel procedure, still enjoys
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some popularity. Flame microanalysis, the Delves cup procedure, applied to blood lead appears
to have an operational sensitivity of about 10 pg Pb/dl blood and a relative precision of
approximately 5 percent 1n the range of blood lead seen in populations in industrialized
areas. The flameless, or electrothermal, method of AAS enhances sensitivity about 10-fold,
but precision can be more problematical because of chemical and spectral interferences.
The most widely used and sensitive electrochemical method for lead in blood 1s anodic
stripping voltamretry (ASV). For most accurate results, chemical wet ashing of samples must
be carried out, although this process 1s time-consuming and requires the use of lead-free rea-
gents. The use of metal exchange reagents has been employed in lieu of the ashing step to li-
berate lead from binding sites, although this substitution is associated with less precision.
For the ashing method, relative precision is approximately 5 percent. In terms of accuracy
and sensitivity, it appears that there are problems at low levels, e.g., 5 Mfl/dl °r below,
particularly if samples contain elevated copper levels.
Lead in plasma. Since lead in whole blood is virtually all confined to the erythrocyte,
plasma levels are quite low and it appears that extreme care must be employed to reliably
measure plasma levels. The best method for such measurement is IDMS, in tandem with ultra-
clean facility use. Atomic absorption spectrometry is satisfactory for comparative analyses
across a range of relatively high whole blood values.
Lead in teeth. Lead measurement in teeth has involved either whole tooth sampling or
analysis of specific regions, such as primary or circumpulpal dentine. In either case, sam-
ples must be solublized after careful surface cleaning to remove contamination; solubilization
is usually accompanied by either wet ashing directly or ashing subsequent to a dry ashing
step.
Atomic absorption spectrometry and anodic stripping have been employed more frequently
for such determinations than any other method. With AAS, the high mineral content of teeth
argues for preliminary isolation of lead via chelation-extraction. The relative precision of
analysis for within-run measurement is around 5-7 percent, with the main determinant of var-
iance in regional assay being the initial isolation step. One change from the usual methods
for such measurement is the in situ measurement of lead by X-ray fluorescence spectrometry in
children. Lead measured 1n this fashion allows observation of on-going lead accumulation, ra-
ther than waiting for exfoliation.
Lead in hair. Hair as an exposure indicator for lead offers the advantages of being non-
invasive and a medium of Indefinite stability. However, there is still the crucial problem of
external surface contamination, which is such that it 1s still not possible to state that any
cleaning protocol reliably differentiates between external and internally deposited lead.
Studies that demonstrate a correlation between increasing hair lead and increasing sever-
ity of a measured effect probably support arguments for hair being an external indicator of
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exposure. It is probably also the case, then, that such measurement, using cleaning protocols
that have not been independently validated, will overstate the relative accumulation of "in-
ternal" hair lead in terms of some endpoint and will also underestimate the relative sensitiv-
ity of changes in internal lead content with exposure. One consequence of this would be, for
example, an apparent threshold for a given effect in terms of hair lead which is significantly
above the actual threshold. Because of these concerns, hair is best used with the simultane-
ous measurement of blood lead.
Lead in urine. Analysis of lead in urine is complicated by the relatively low levels of
the element in this medium as well as the complex mixture of mineral elements present. Urine
lead levels are most useful and also somewhat easier to determine in cases of chelation mobil-
ization or chelation therapy, where levels are high enough to permit good precision and dilu-
tion of matrix interference.
Samples are probably best analyzed by prior chemical wet ashing, using the usual mixture
of acids. Both anodic stripping voltammetry and atomic absorption spectrometry have been ap-
plied to urine analysis, with the latter more routinely used and usually with a chelation/
extraction step.
Lead in other tissues. Bone samples require cleaning procedures for removal of muscle
and connective tissue and chemical solubilization prior to analysis. Methods of analysis are
comparatively limited and it appears that flameless atomic absorption spectrometry is the
technique of choice.
Lead measurements in bone, in vivo, have been reported with lead workers, using x-ray
fluorescence analysis and a radioisotopic source for excitation. One problem with this
approach with moderate lead exposure is the detection limit, approximately 20 ppm. Soft organ
analysis poses a problem in terms of heterogeneity of lead distribution within an organ, e.g.,
brain and kidney. In such cases, regional sampling or homogenization must be carried out.
Both flame and flameless atomic absorption spectrometry appear to be satisfactory for soft
tissue analysis and are the most widely used.
Quality assurance procedures in lead analyses. In terms of available information, the
major focus in establishing quality control protocols for lead has involved whole blood meas-
urements. Translated into practice, quality control revolves around steps employed within the
laboratory, using a variety of internal checks, and the further reliance on external checks,
such as a formal continuing multl-laboratory proficiency testing program.
Within the laboratory, quality assurance protocols can be divided into start-up and rou-
tine procedures, the former involving establishment of detection limits, within-run and
between-run precision, analytical recovery, and comparison with some reference technique
within or outside the laboratory. The reference method is assumed to be accurate for the par-
ticular level of lead in some matrix at a particular point in time. Correlation with such a
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method at a satisfactory level, however, may simply indicate that both methods are equally
Inaccurate but performing with the same level of precision proficiency. More preferable is
the use of certified samples having lead at a level established by the definitive method.
For blood lead, the Centers for Disease Control periodically survey overall accuracy and
precision of methods used by reporting laboratories. In terms of overall accuracy and preci-
sion, one such survey found that anodic stripping voltaimnetry as well as the Delves cup and
extraction variations of atomic absorption spectrometry performed better than other proce-
dures. These results do not mean that a given laboratory cannot perform better with a partic-
ular technique; rather, such data are of assistance for new facilities choosing among methods.
Of particular value to laboratories carrying out blood lead analysis are the external
quality assurance programs at both the state and federal levels. The most comprehensive pro-
ficiency testing program is that carried out by the Centers for Disease Control, USPHS. This
program actually consists of two subprograms, one directed at facilities involved in lead poi-
soning prevention and screening (Center for Environmental Health) and the other concerned with
laboratories seeking certification under the Clinical Laboratories Improvement Act of 1967 as
well as under regulations of the Occupational Safety and Health Administration's (OSHA) Labor-
atory Improvement Program Office. Overall, the proficiency testing programs have served their
purpose well, judging from the relative overall improvements in reporting laboratories over
the years of the programs' existence. In this regard, OSHA criteria for laboratory certifica-
tion require 8 of 9 samples be correctly analyzed for the previous quarter. This level of
required proficiency reflects the ability of a number of laboratories to actually perform at
this level.
1.9.2 Determination of Erythrocyte Porphyrin (Free Erythrocyte Protoporphyrin, Zinc
Protoporphyrin)
With lead exposure, there 1s an accumulation of erythrocyte protoporphyrin IX, owing to
impaired placement of divalent iron to form heme. Divalent zinc occupies the place of the na-
tive iron. Depending upon the method of analysis, either metal-free erythrocyte porphyrin or
zinc protoporphyrin (ZPP) Is measured, the former arising from loss of zinc 1n the chemical
manipulation. Virtually all methods now in use for EP analysis exploit the ability of the
porphyrin to undergo intense fluorescence when excited by ultraviolet light. Such fluoro-
metric methods can be further classified as wet chemical mlcromethods or direct measuring
fluorometry using the hematofluorometer. Owing to the high sensitivity of such measurement,
relatively small blood samples are required, with liquid samples or blood collected on filter
paper.
The most common laboratory or wet chemical procedures now 1n use represent variations of
several common chemical procedures: (1) treatment of blood samples with a mixture of ethyl
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acetate/acetic acid followed by a repartitioning into an Inorganic acid medium, or (2) solu-
bilization of a blood sample directly into a detergent/buffer solution at a high dilution.
Quantification has been done using protoporphyrin, coproporphyria or zinc protoporphyrin IX
plus pure zinc ion. The levels of precision for these laboratory techniques vary somewhat
with the specifics of analysis. The Piomelli method has a coefficient of variation of 5
percent, while the direct ZPP method using buffered detergent solution is higher and more
variable.
The recent development of the hematofluorometer has made it possible to carry out EP mea-
surements in high numbers, thereby making population screening feasible. Absolute calibration
is necessary and requires periodic adjustment of the system using known concentrations of EP
in reference blood samples. Since these units are designed for oxygenated blood, i.e.,
capillary blood, use of venous blood requires an oxygenation step, usually a moderate shaking
for several minutes. Measurement of low or moderate levels of EP can be affected by inter-
ference with bilirubin. Competently employed, the hematofluorometer appears to be reasonably
precise, showing a total coefficient of variation of 4.11-11.5 percent. While the comparative
accuracy of the unit has been reported to be good relative to the reference wet chemical
technique, a very recent study has shown that commercial units carry with them a significant
negative bias, which may lead to false negatives in subjects having only moderate EP
elevation. Such a bias in accuracy has been difficult to detect in existing EP proficiency
testing programs. It appears that, by comparlsion to wet methods, the hematofluorometer
should be restricted to field use rather than becoming a substitute in the laboratory for
chemical measurement, and field use should involve periodic split-sample comparison testing
with the wet method.
1.9.3 Measurement of Urinary Coproporphyria
Although EP measurement has largely supplanted the use of urinary coproporphyrln analysis
(CP-U) to monitor excessive lead exposure in humans, this measurement is still of value in
that it reflects active intoxication. The standard analysis is a fluorometric technique,
whereby urine samples are treated with buffer, and an oxidant (iodine) is added to generate CP
from its precursor. The CP-U is then partitioned into ethyl acetate and re-extracted with
dilute hydrochloric acid. The working curve is linear below 5 (jg CP/dl urine.
1.9.4 Measurement of Delta-Aminolevulinic Acid Oehydrase Activity
Inhibition of the activity of the erythrocyte enzyme, delta-aminolevulinic acid dehydrase
(ALA-D), by lead is the basis for using such activity in screening for excessive lead expo-
sure. A number of sampling and sample handling precautions attend such analysis. Since zinc
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(II) ion will offset the degree of activity inhibition by lead, blood collecting tubes Mist
have extremely low zinc content. This essentially rules out the use of rubber-stoppered blood
tubes. Enzyme stability is such that the activity measurement is best carried out within 24
hours of blood collection. Porphobilinogen, the product of enzyme action, is light-labile and
requires the assay be done in restricted light. Various procedures for ALA-D Measurement are
based on measurement of the level of the chrowophoric pyrrole (approximately 555 mi) formed by
condensation of the porphobilinogen with p-d i methyl ami nobenza1dehyde.
In the European Standardized Method for ALA-D activity determination, blood samples are
hemolyzed with water, ALA solution added, followed by incubation at 37°C, and the reaction
terminated by a solution of mercury (II) in trichloroacetic acid. Filtrates are treated with
modified Ehrlich's reagent (p-dlmethylaminobenzaldehyde) in trichloroacetic/perchloroacetic
acid mixture. Activity is quantified in terms of micromoles ALA/min/liter erythrocytes.
One variation in the above procedure is the initial use of a thiol agent, such as dithio-
threotol, to reactivate the enzyme, giving a measure of the full native activity of the
enzyme. The ratio of activated/unactivated activity vs. blood lead levels accomodates genetic
differences between individuals.
1.9.5 Measurement of Delta-Aminolevulinic Acid in Urine and Other Hedia
Levels of delta-aminolevulinic acid (6-ALA) in urine and plasma increase with elevated
lead exposure. Thus, measurement of this metabolite, generally in urine, provides an index of
the level of lead exposure. ALA content of urine samples (ALA-U) is stable for about two
weeks or more with sample acidification and refrigeration. Levels of ALA-U are adjusted for
urine density or expressed per unit creatinine. If feasible, 24-hour collection is more
desirable than spot sampling.
Virtually all the various procedures for ALA-U measurement employ preliminary isolation
of ALA from the balance of urine constituents. In one method, further separation of ALA from
the metabolite aminoacetone is done. Aminoacetone can interfere with colorimetric measure-
ment. ALA is recovered, condensed with a beta-dlcarbonyl compound, e.g., acetyl acetone, to
yield a pyrrole intermediate. This intermediate is then reacted with p-dimethylaminobenzalde-
hyde in perchloric/acetic acid, followed by colorimetric reading at 553 nm. In one variation
of the basic methodology, ALA is condensed with ethyl acetoacetate directly and the resulting
pyrrole extracted with ethyl acetate. Ehrlich's reagent is then added as in other procedures
and the resulting chromophore measured spectrophotometrically.
Heasurement of ALA in plasma is much more difficult than in urine, since plasma ALA is at
nanogram/milliter levels. In one gas-l1quid chromatographic procedure, ALA is isolated from
plasma, reacted with acetyl acetone and partitioned into a solvent that also serves for pyro-
lytic methylation of the involatile pyrrole 1n the injector port of the chromatograph, making
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the derivative more volatile. For quantification, an interval standard, 6-amino-5-oxohixanoic
acid, is used. While the method is more involved, it is more specific than the older colori-
aetric technique.
1.9.6 Measurement of Pyriaidine-5'-Nucleotidase Activity
Erythrocyte pyr1*1d1ne-5'-nucleotidase (Py5N) activity is inhibited with lead exposure.
Presently two different methods are used for assaying the activity of this enzyme. The older
method is quite laborious in time and effort, whereas the lore recent approach is shorter but
uses radioisotopes and radiometric measurement.
In the older method, heparin!zed venous blood is filtered through cellulose to separate
erythrocytes from platelets and leukocytes. Cells are then freeze-fractured and the hemoly-
sates dialyzed to remove nucleotides and other phosphates. This dialysate is then incubated
in the presence of a nucleoside monophosphate and cofactors, the enzyme reaction being termi-
nated by treatment with trichloroacetic acid. The inorganic phosphate isolated from added
substrate is measured colorimetrically as the phosphomolybdic acid complex.
14
In the radiometric assay, hemolysates obtained as before are incubated with pure C-CMP.
By addition of a barium hydroxide/zinc sulfate solution, proteins and unreacted nucleotide are
14
precipitated, leaving labeled cytidine in the supernatant. Aliquots are measured for C ac-
tivity in a liquid scintillation counter. This method shows a good correlation with the ear-
lier technique.
1.10 METABOLISM OF LEAD
Toxicokinetic parameters of lead absorption, distribution, retention, and excretion con-
necting external environmental lead exposure to various adverse effects are discussed in this
section. Also considered are various influences on these parameters, e.g., nutritional
status, age, and stage of development.
A number of specific issues in lead metabolism by animals and humans merit special focus
and these include:
1. How does the developing organism from gestation to maturity differ from the
adult in toxicokinetic response to lead intake?
2. What do these differences in lead metabolism portend for relative risk for
adverse effects?
3. What are the factors, that significantly change the toxicokinetic parameters in
ways relevant to assessing health risk?
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4. How do the various interrelationships among body compartments for lead trans-
late to assessment of internal exposure and changes in internal exposure?
1,10.1 Lead Absorption in Humans and Animals
The amounts of lead entering the bloodstream via various routes of absorption are influ-
enced not only by the levels of the element in a given medium but also by various physical and
chemical parameters and specific host factors, such as age and nutritional status.
Respiratory absorption of lead. The movement of lead from ambient air to the blood-
stream is a two-part process: deposition of some fraction of inhaled air lead in the deeper
part of the respiratory tract and absorption of the deposited fraction. For adult humans, the
deposition rate of particulate airborne lead as likely encountered by the general population
is around 30-50 percent, with these rates being modified by such factors as particle size and
ventilation rates. It also appears that essentially all of the lead deposited in the lower
respiratory tract is absorbed, so that the overall absorption rate is governed by the deposi-
tion rate, i.e., approximately 30-50 percent. Autopsy results showing no lead accumulation in
the lung indicate quantitative absorption of deposited lead.
All of the available data for lead uptake via the respiratory tract in humans have been
obtained with adults. Respiratory uptake of lead in children, while not fully quantifiable,
appears to be comparatively greater on a body weight basis, compared to adults. A second fac-
tor influencing the relative deposition rate in children has to do with airway dimensions.
One report has estimated that the 10-year-old child has a deposition rate 1.6- to 2.7-fold
higher than the adult on a weight basis.
It appears that the chemical form of the lead compound inhaled is not a major determinant
of the extent of alveolar absorption of lead. While experimental animal data for quantitative
assessment of lead deposition and absorption for the lung and upper respiratory tract are lim-
ited, available information from the rat, rabbit, dog, and nonhuman primate support the find-
ings that respired lead in humans is extensively and rapidly absorbed.
Gastrointestinal absorption of lead. Gastrointestinal absorption of lead mainly involves
lead uptake from food and beverages as well as lead deposited in the upper respiratory tract,
which is eventually swallowed. It also includes ingestion of non-food material, primarily in
children via normal mouthing activity and pica. Two issues of concern with lead uptake from
the gut are the comparative rates of such absorption in developing vs. adult organisms,
including humans, and how the relative bioavailability of lead affects such uptake.
By use of metabolic balance and isotopic (radioisotope or stable isotope) studies, var-
ious laboratories have provided estimates of lead absorption in the human adult on the order
of 10-15 percent. This rate can be significantly increased under fasting conditions to 45
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percent, compared to lead Ingested with food. The latter figure also suggests that beverage
lead is absorbed to a greater degree since much beverage ingestion occurs between meals.
The relationship of the chemical/biochemical form of lead in the gut to absorption rate
has been studied, although interpretation is complicated by the relatively small amounts given
and the presence of various components in food already present in the gut. In general, how-
ever, chemical forms of lead or their incorporation into biological matrices seems to have a
minimal impact on lead absorption in the human gut. Several studies have focused on the ques-
tion of differences in gastrointestinal absorption rates for lead between children and adults.
It would appear that such rates for children are considerably higher than for adults: 10-15
percent for adults vs. approximately 50 percent for children. Available data for the absorp-
tion of lead from non-food items such as dust and dirt on hands are limited, but one study has
estimated a figure of 30 percent. For paint chips, a value of about 17 percent has been esti-
mated.
Experimental animal studies show that, like humans, the adult absorbs much less lead from
the gut than the developing animal. Adult rats maintained on ordinary rat chow absorb 1 per-
cent or less of the dietary lead. Various animal species studies make It clear that the new-
born absorbs a much greater amount of lead than the adult, supporting studies showing this age
dependency in humans. Compared to an absorption rate of approximately 1 percent in adult
rats, the rat pup has a rate 40-50 times greater. Part, but not most, of the difference can
be ascribed to a difference in dietary composition. In nonhuman primates, infant monkeys
absorb 65-85 percent of lead from the gut, compared to 4 percent for the adults.
The bioavailability of lead in the gastrointestinal (GI) tract as a factor in its absorp-
tion has been the focus of a number of experimental studies. These data show that: (1) lead
in a number of forms is absorbed about equally, except for the sulfide; (2) lead in dirt and
dust and as different chemical forms is absorbed at about the same rate as pure lead salts
added to the diet; (3) lead in paint chips undergoes significant uptake from the gut; and
4) in some cases, physical size of particulate lead can affect the rate of GI absorption.
Percutaneous absorption of lead. Absorption of inorganic lead compounds through the skin
is of much less significance than through the respirator and gastrointestinal routes. This
is in contrast to the case with lead alkyls (See Section 1.10.6). One recent study using
203
human volunteers and Pb-labeled lead acetate showed that under normal conditions, absorp-
tion approaches 0.06 percent.
Transplacental transfer of lead. Lead uptake by the human and animal fetus readily
occurs, such transfer going on by the 12th week of gestation in humans, with increasing fetal
uptake throughout development. Cord blood contains significant amounts of lead, correlating
with but somewhat lower than maternal blood lead levels. Evidence for such transfer, besides
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lead content of cord blood, includes fetal tissue analyses and reduction in naternal blood
lead during pregnancy. There also appears to be a seasonal effect on the fetus, summer-born
children showing a trend toward higher blood lead levels than those born in the spring.
1.10.2 Distribution of Lead in Humans and Animals
In this subsection, the distributional characteristics of lead in various portions of the
body—blood, soft tissue, calcified tissue, and the "chelatable" or potentially toxic body
burden—are discussed as a function of such variables as exposure history and age.
1.10.2.1 Lead in Blood. More than 99 percent of blood lead is associated with the erythro-
cyte in humans under steady-state conditions, but it is the very small fraction transported in
plasma and extracellular fluid that provides lead to the various body organs. Most (-v 50 per-
cent) of erythrocyte lead 1s bound within the cell, primarily associated with hemoglobin (par-
ticularly HbA^), with approximately 5 percent bound to a 10,000-dalton fraction, 20 percent to
a heavier molecule, and 25 percent to lower weight species.
Whole blood lead 1n daily equilibrium with other compartments 1n adult humans appears to
have a biological half-time of 25-28 days and comprises about 1.9 mg in total lead content.
Human blood lead responds rather quickly to abrupt changes in exposure. With increased lead
intake, blood lead achieves a new value in approximately 40-60 days, while a decrease In expo-
sure may be associated with variable new blood values, depending upon the exposure history.
This dependence presumably reflects lead resorption from bone. With age, furthermore, there
appears to be little change in blood lead during adulthood. Levels of lead in blood of chil-
dren tend to show a peaking trend at 2-3 years of age, probably due to mouthing activity, fol-
lowed by a decline. In older children and adults, levels of lead are sex-related, females
showing lower levels than men even at comparable levels of exposure.
In plasma, lead is virtually all bound to albumin and only trace amounts to high weight
globulins. It is not possible to state which binding form constitutes an "active" fraction
for movement to tissues. The most recent studies of the erythrocyte-plasna relationship in
humans indicate that there is an equilibrium between these blood compartments, such that
levels in plasma rise with levels in whole blood.
1.10.2.2 Lead Levels in Tissues. Of necessity, various relationships of tissue lead to expo-
sure and toxicity in humans must generally be obtained from autopsy samples. Limitations on
such data include questions of how samples represent lead behavior in the living population,
particularly with reference to prolonged illness and disease states. The adequate characteri-
zation of exposure for victims of fatal accidents is a problem, as is the fact that such stud-
ies are cross-sectional in nature, with different age groups assumed to have had similar ex-
posure in the past.
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Soft tissues. After age 20, most soft tissues in humans do not show age-related changes,
in contrast to bone. Kidney cortex shows increase in lead with age which may be associated
with formation of nuclear inclusion bodies. Absence of lead accumulation in most soft tissues
is due to a turnover rate for lead which is similar to that in blood.
Based on several autopsy studies, it appears that soft tissue lead content for individ-
uals not occupational1y exposed is generally below 0.5 pg/g wet weight, with higher values for
aorta and kidney cortex. Brain tissue lead level is generally below 0.2 ppm wet weight with
no change with increasing age, although the cross-sectional nature of these data would make
changes in low brain lead levels difficult to discern. Autopsy data for both children and
adults indicate that lead is selectively accumulated in the hippocampus, a finding that is
also consistent with the reginal distribution in experimental animals.
Comparisons of lead levels in soft tissue autopsy samples from children with results from
adults indicate that such values are lower in infants than in older children, while children
aged 1-16 years had levels comparable to adult women. In one study, lead content of brain re-
gions did not materially differ for infants and older children compared to adults. Complicat-
ing these data somewhat are changes in tissue mass with age, although such changes are less
than for the skeletal system.
Subcellular distribution of lead in soft tissue is not uniform, with high amounts of lead
being sequestered in the mitochondria and nucleus. Nuclear accumulation is consistent with
the existence of lead-containing nuclear inclusions in various species and a large body of
data demonstrating the sensitivity of mitochondria to injury by lead.
Mineralizing tissue. Lead becomes localized and accumulates in human calcified tissues,
i.e., bones and teeth. This accumulation in humans begins with fetal development and contin-
ues to approximately 60 years of age. The extent of lead accumulation in bone ranges up to
200 mg in men ages 60-70 years, while in women lower values have been measured. Based upon
various studies, approximately 95 percent of total body lead is lodged in the bones of human
adults, with uptake distributed over trabecular and compact bone. In the human adult, bone
lead is both the most inert and largest body pool, and accumulation can serve to maintain el-
evated blood lead levels years after exposure, particularly occupational exposure, has ended.
Compared to the human adult, 73 percent of body lead is lodged in the bones of children,
which is consistent with other information that the skeletal system of children is more meta-
bolically active than in the adult. While the increase in bone lead across childhood is mod-
est, about 2-fold if expressed as concentration, the total accumulation rate is actually 80-
fold, taking into account a 40-fold increase in skeletal mass. To the extent that some sig-
nificant fraction of total bone-lead in children and adults is relatively labile, it is more
appropriate in terms of health risk for the whole organism to consider the total accumulation
rather than just changes in concentration.
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The traditional view that the skeletal system was a "total" sink for body lead (and by
implication a biological safety feature to permit significant exposure in industrialized popu-
lations) never did accord with even older Information on bone physiology, e.g., bone remodel-
ling, and is now giving way to the view that there are at least several bone compartments for
lead, with different nobility profiles. It would appear, then, that "bone lead" may be more
of an insidious source of long-term internal exposure than a sink for the element. This
aspect of the issue is summarized more fully in the next section. Available information from
studies of such subjects as uranium miners and human volunteers ingesting stable isotopes in-
dicates that there is a relatively inert bone compartment for lead, having a half-time of sev-
eral decades, and a rather labile compartment which permits an equilibrium between bone and
tissue lead.
Tooth lead also increases with age at a rate proportional to exposure and roughly propor-
tional to blood lead in humans and experimental animals. Dentine lead is perhaps the most re-
sponsive component of teeth to lead exposure since It is laid down from the time of eruption
until shedding. It is this characteristic which underlies the utility of dentine lead levels
in assessing long-term exposure.
Chelatable lead. Mobile lead in organs and systems is potentially more active toxicolog-
ically in terms of being available to biological sites of action. Hence, this fraction of
total boc(y lead burden is a more significant predictor of imminent toxicity. In reality,
direct measurement of such a fraction in human subjects would not be possible. In this
regard, "chelatable" lead, measured as the extent of plumburesis in response to administration
of a chelating agent, is now viewed as the most useful probe of undue body burden in children
and adults.
A quantitative description of the inputs to the body lead fraction that is chelant-
mobilizable is difficult to fully define, but it most likely includes a labile lead compart-
ment within bone as well as in soft tissues. Support for this view Includes: (1) the age de-
pendency of chelatable lead, but not lead in blood or soft tissues; (2) evidence of removal of
bone lead in chelation studies with experimental animals; (3) in vitro studies of lead mobili-
zation in bone organ explants under closely defined conditions; (4) tracer modelling estimates
in human subjects; and (5) the complex nonlinear relationship of blood lead and lead intake
through various media. Data for children and adults showing a logarithmic relationship of
chelatable lead to blood lead and the phenomenon of "rebound" in blood lead elevation after
chelation therapy regimens (without obvious external re-exposure) offer further support.
Animal studies. Animal studies have been of help in sorting out some of the relation-
ships of lead exposure to in vivo distribution of the element, particularly the impact of
skeletal lead on whole body retention. In rats, lead administration results 1n an Initial in-
crease in soft tissues, followed by loss from soft tissue via excretion and transfer to bone.
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Lead distribution appears to be relatively independent of dose. Other studies have shown that
lead loss from organs follows first-order kinetics except for bone, and the skeletal system in
rats and mice is the kinetically rate-limiting step in whole-body lead clearance.
The neonatal animal seems to retain proportionally higher levels of tissue lead compared
to the adult and manifests slow decay of brain lead levels while showing a significant decline
over time in other tissues. This appears to be the result of enhanced lead entry into the
brain because of a poorly developed blood-brain barrier system as well as enhanced body reten-
tion of lead by young animals.
The effects of such changes as metabolic stress and nutritional status on body redistri-
bution of lead have been noted. Lactating mice, for example, are known to demonstrate tissue
redistribution of lead, specifically bone lead resorption with subsequent transfer of both
lead and calcium from mother to pups,
1.10.3 Lead Excretion and Retention in Humans and Animals
Human studies. Dietary lead in humans and animals that is not absorbed passes through
the gastrointestinal tract and is eliminated with feces, as is the fraction of air lead that
is swallowed and not absorbed. Lead entering the bloodstream and not retained is excreted
through the renal and GI tracts, the latter via biliary clearance. The amounts excreted
through these routes are a function of such factors as species, age, and exposure character-
istics.
Based upon the human metabolic balance data and isotope excretion findings of various in-
vestigators, it appears that short-term lead excretion in adult humans amounts to 50-60 per-
cent of the absorbed fraction, with the balance moving primarily to bone and some fraction
(approximately half) of this stored amount eventually being excreted. This overall retention
figure of 25 percent necessarily assumes that isotope clearance reflects that for body lead in
all compartments. The rapidly excreted fraction has a biological half-time of 20-25 days,
similar to that for lead removal from blood. This similarity indicates a steady rate of lead
clearance from the body. In terms of partitioning of excreted lead between urine and bile,
one study indicates that the biliary clearance is about 50 percent that of renal clearance.
Lead is accumulated in the human body with age, mainly in bone, up to around 60 years of
age, when a decrease occurs with changes in intake as well as in bone mineral metabolism. As
noted earlier, the total amount of lead in long-term retention can approach 200 mg, and even
much higher in the case of occupational exposure. This corresponds to a lifetime average
retention rate of 9-10 Pg/day. Within shorter time frames, however, retention will vary
considerably due to such factors as development, disruption in the individuals' equilibrium
with lead intake, and the onset of such states as osteoporosis.
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The age dependency of lead retention/excretion In humans has not been well studied, but
most of the available information indicates that children, particularly infants, retain a sig-
nificantly higher amount of lead. While autopsy data indicate that pediatric subjects at iso-
lated points in time actually have a lower fraction of body lead lodged in bone, a full under-
standing of longer-term retention over childhood must consider the exponential growth rate oc-
curring in a child's skeletal system over the time period for which bone lead concentrations
have been gathered. This parameter itself represents a 40-fold mass increase. This signifi-
cant skeletal growth rate has an impact on an obvious question: if children take in more lead
on a body weight basis than adults, absorb and retain more lead than adults, and show, only
modest elevations in blood lead compared to adults in the face of a more active skeletal sys-
tem, where does the lead go? A second factor is the assumption that blood lead in children
relates to body lead burden in the sane quantitative fashion as in adults, an assumption that
remains to be adequately proven.
Animal studies. In rats and other experimental animals, both urinary and fecal excretion
appear to be important routes of lead removal from the organism; the relative partitioning
between the two modes is species- and dose-dependent. With regard to species differences,
biliary clearance of lead in the dog is but 2 percent of that for the rat, while such excre-
tion in the rabbit 1s 50 percent that of the rat.
Lead movement from laboratory animals to their offspring via milk constituents is a route
of excretion for the mother as well as an exposure route for the young. Comparative studies
of lead retention in developing vs. adult animals, e.g., rats, mice, and non-human primates,
make it clear that retention is significantly greater in the young animal. These observations
support those studies showing greater lead retention in children. Some recent data indicate
that a differential retention of lead in young rats persists into the post-weaning period,
calculated as either uniform dosing or uniform exposure.
1.10.4 Interactions of Lead with Essential Metals and Other Factors
Toxic elements such as lead are affected in their toxicokinetic or toxicological behavior
by interactions with a variety of biochemical factors such as nutrients.
Human studies. In humans the interactive behavior of lead and various nutritional fac-
tors is expressed most significantly in young children, with such interactions occurring
against a backdrop of rather widespread deficiencies in a number of nutritional components.
Various surveys have indicated that deficiency in iron, calcium, zinc, and vitamins are wide-
spread among the pediatric population, particularly the poor. A number of reports have docu-
mented the association of lead absorption with suboptimal nutritional states for iron and cal-
cium, reduced Intake being associated with increased lead absorption.
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Animal studies. Reports of lead-nutrient interactions in experimental animals have
generally described such relationships for a single nutrient, using relative absorption or
tissue retention in the animal to index the effect. Most of the recent data are for calcium,
iron, phosphorus, and vitamin D. Many studies have established that diminished dietary cal-
cium is associated with increased blood and soft tissue lead content in such diverse species
as the rat, pig, horse, sheep, and domestic fowl. The increased body burden of lead arises
from both increased GI absorption and increased retention, indicating that the lead-calcium
interaction operates at both the gut wall and within body compartments. Lead appears to tra-
verse the gut via both passive and active transfer, involves transport proteins normally oper-
ating for calcium transport, and is taken up at the site of phosphorus, not calcium, absorp-
tion.
Iron deficiency is associated with an increase in lead of tissues and Increased toxicity,
an effect which is expressed at the level of lead uptake by the gut wall. In vitro studies
Indicate an Interaction through receptor binding competition at a common site. This probably
involves iron-binding proteins. Similarly, dietary phosphate deficiency enhances the extent
of lead retention and toxicity via increased uptake of lead at the gut wall, both lead and
phosphate being absorbed at the same site In the small intestine. Results of various studies
of the resorption of phosphate along with lead as one further mechanism of elevation of tissue
lead have not been conclusive. Since calcium plus phosphate retards lead absorption to a
greater degree than simply the sums of the Interactions, it has been postulated that an insol-
uble complex of all these elements may be the basis of this retardation.
Unlike the inverse relationship existing for calcium, iron, and phosphate vs. lead
uptake, vitamin D levels appear to be directly related to the rate of lead absorption from the
GI tract, since the vitamin stimulates the same region of the duodenum where lead Is absorbed.
A number of other nutrient factors are known to have an interactive relationship with lead:
1. Increases in dietary lipids increase the extent of lead absorption, with the
extent of the increase being highest with polyunsaturates and lowest with satu-
rated fats, e.g., tristearin.
2. The interactive relationship of lead and dietary protein is not clearcut, and
either suboptimal or excess protein Intake increases lead absorption.
3. Certain milk components, particularly lactose, also greatly enhance lead ab-
sorption in the nursing animal.
4. Zinc deficiency promotes lead absorption, as does reduced dietary copper.
1.10.5 Interrelationships of Lead Exposure with Exposure Indicators and Tissue Lead Burdens
There are three issues involving lead toxicokinetics which bear importantly on the char-
acterization of relationships between lead exposure and its toxic effects: (1) the temporal
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characteristics of internal indices of lead exposure; (2) the biological aspects of the rela-
tionship of lead in various environnental media to various indicators of internal exposure;
and (3) the relationship of various internal indicators of exposure to target tissue lead bur-
dens.
Temporal characteristics of internal indicators of lead exposure. The biological half-
time for newly absorbed lead in blood appears to be of the order of weeks or several months,
so that this medium reflects relatively recent exposure. If recent exposure is fairly repre-
sentative of exposure over a considerable period of tine, e.g., exposure of lead workers, then
blood lead is more useful than for cases where exposure 1s intermittent across time, as 1s
often the case of pediatric lead exposure. Accessible mineralized tissue, such as shed teeth,
extend the time frame back to years of exposure, since teeth accumulate lead with age and as a
function of the extent of exposure. Such measurements are, however, retrospective in nature,
in that identification of excessive exposure occurs after the fact and thus limits the possi-
bility of timely medical intervention, exposure abatement, or regulatory policy concerned with
ongoing control strategies.
Perhaps the most practical solution to the dilemma posed by both tooth and blood lead
analyses is in situ measurement of lead in teeth or bone during the time when active accumu-
lation occurs, e.g., 1n 2 to 3-year-old children. Available data using X-ray fluorescence
analysis suggest that such approaches are feasible and can be reconciled with such issues as
acceptable radiation hazard risk to subjects.
Biological aspects of external exposure-internal Indicator relationships. It is clear
from a reading of the literature that the relationship of lead in relevant media for human ex-
posure to blood lead is curvilinear when viewed over a relatively broad range of blood lead
values. This implies that the unit change in blood lead per unit intake of lead in some
medium varies across this range of exposure, with comparatively smaller blood lead changes as
internal exposure increases.
Given our present knowledge, such a relationship cannot be taken to mean that body uptake
of lead 1s proportionately lower at higher exposure, for it may simply mean that blood lead
becomes an Increasingly unreliable measure of target tissue lead burden with increasing expo-
sure. While the basis of the curvilinear relationship remains to be identified, available an-
imal data suggest that it does not reflect exposure-dependent absorption or excretion rates.
Internal indicator-tissue lead relationships. In living human subjects, it 1s not possi-
ble to determine directly tissue lead burdens or how these relate to adverse effects in target
tissues; some accessible indicator, e.g., lead in a medium such as blood or a biochemical sur-
rogate of lead such as EP, must be employed. While blood lead still remains the only practi-
cal measure of excessive lead exposure and health risk, evidence continues to accumulate that
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such an index has limitations in either reflecting tissue lead burdens or changes in such tis-
sues with changes in exposure.
At present, the measurement of plumburesis associated with challenge by a single dose of
a lead chelating agent such as GaNa2E0TA is considered the best indicator of the mobile, po-
tentially toxic fraction of body lead. Chelatable lead is logarithmically related to blood
lead, such that incremental Increase in blood lead is associated with an Increasingly larger
increment of mobilizable lead. The problems associated with this logarithmic relationship may
be seen in studies of children and lead workers in whom moderate elevation in blood lead can
disguise levels of mobile body lead. This reduces the margin of protection against severe in-
toxication. The biological basis of the logarithmic relationship between chelatable lead and
blood lead rests, in large measure, with the existence of a sizable bone lead compartment that
is mobile enough to undergo chelation removal and, hence, potentially mobile enough to move
into target tissues.
Studies of the relative mobility of chelatable lead over time indicate that, in former
lead workers, removal from exposure leads to a protracted washing out of lead (from bone re-
sorption of lead) to blood and tissues, with preservation of a bone burden amenable to subse-
quent chelation. Studies with children are inconclusive, since the one investigation directed
to this end employed pediatric subjects who all underwent chelation therapy during periods of
severe lead poisoning. Animal studies demonstrate that changes in blood lead with increasing
exposure do not agree with tissue uptake in a time-concordant fasion, nor does decrease in
blood lead with reduced exposure signal a similar decrease in target tissue, particularly in
the brain of the developing organism.
1.10.6 Metabolism of Lead AlkyIs
The lower alkyl lead components used as gasoline additives, tetraethyl lead (TEL) and
tetramethyl lead (TML), may themselves poise a toxic risk to humans. In particular, there 1s
among children a problem of sniffing leaded gasoline.
Absorption of lead alkyls in humans and animals. Human volunteers inhaling labeled TEL
and TML show lung deposition rates for the lead alkyls of 37 and 51 percent, respectively,
values which are similar to those for particulate inorganic lead. Significant portions of
these deposited amounts were eventually absorbed. Respiratory absorption of organolead bound
to particulate matter has not been specifically studied as such.
While specific data for the GI absorption of lead alkyls in humans and animals are not
available, their close similarity to organotin compounds, which are quantitatively absorbed,
would argue for extensive GI absorption. In contrast to inorganic lead salts, the lower lead
alkyls are extensively absorbed through the skin and animal data show lethal effects with per-
cutaneous uptake as the sole route of exposure.
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Biotransformation and tissue distribution of lead alkyls. The lower lead alkyls TEL and
TML undergo monodealkylation in the liver of mammalian species via the P-450-dependent mono-
oxygenase enzyme system. Such transformation is very rapid. Further transformation involves
conversion to the dialkyl and inorganic lead forms, the latter accounting for the effects on
heme biosynthesis and erythropoiesis observed in alky! lead intoxication. Alykl lead is
rapidly cleared from blood, shows a higher partitioning into plasma than inorganic lead with
triethyl lead clearance being more rapid than the methyl analog.
Tissue distribution of alky! lead in humans and animals primarily involves the trialkyl
metabolites, levels are highest in liver, followed by kidney, then brain. Of interest is the
fact that there are detectable amounts of trialkyl lead from autopsy samples of human brain
even in the absence of occupational exposure. In humans, there appear to be two tissue com-
partments for triethyl lead, having half-times of 35 and 100 days.
Excretion of lead alkyls. With alkyl lead exposure, excretion of lead through the renal
tract is the main route of elimination. The chemical forms being excreted appear to be
species-dependent. In humans, trialkyl lead in workers chronically exposed to alkyl lead is a
minor component of urine lead, approximately 9 percent.
1.11. ASSESSMENT OF LEAD EXPOSURES AND ABSORPTION IN HUMAN POPULATIONS
Chapter 11 describes the effect of exposure of human populations to lead in their en-
vironment. The effect discussed is a change in an internal exposure index that follows changes
in external exposures. The index of internal lead exposure most frequently cited is blood
lead levels, but other indices such as levels of lead in tooth and bone are also presented.
Blood lead level estimates the body's recent exposure to environmental lead, while teeth and
bone lead levels represent cumulative exposures.
Measurement of lead in blood has been accomplished via a succession of analytical proce-
dures over the years. With these changes in technology there has been increasing recognition
of the importance of controlling for contamination in the sampling and analytical procedures.
These advances as well as the institution of external quality control programs have resulted
in markedly improved analytic results. A generalized improvement in analytic results across
many laboratories occurred during Federal Fiscal Years 1977-1979.
The main discussion of scientific evidence in Chapter 11 is structured to achieve four
main objectives:
(1) Elucidate patterns of absorbed lead in U.S. populations and identify important
demographic covariates.
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(2) Characterize relationships between external and internal exposures by exposure
medium.
(3) Define the relative contributions of various sources of lead in the environment
to total internal exposure.
(4) Identify specific sources of lead which result in increased Internal exposure
levels.
A question of major interest in understanding environmental pollutants is the extent to
which current ambient exposures exceed background levels. Ancient Nubians samples (dated
3300-2900 B.C.) averaged 0.6 Mi lead/g for bone and 0.9 pg lead/g for teeth. More recent
Peruvian Indian samples (12th Century) had teeth lead levels of 13.6 pg/g. Contemporary
Alaskan Eskimo samples had a mean of 56.0 pg/g, while Philadelphia samples had a mean of 188.3
pg/g. These data suggest an increasing pattern of lead absorption.
Several studies have looked at the blood lead levels in current remote populations such
as natives in a remote (far from industrialized regions) section of Nepal where the lead con-
3
tent of the air samples proved to be less than the detection limit, 0.004 pg/m (Piomelli et
al., 1980). The geometric mean blood lead for this population was 3.4 pg/dl. Adult males had
a geometric mean of 3.8 pg/dl and adult females, 2.9 pg/dl. Children had a geometric mean
blood lead of 3.5 pg/dl.
1.11.1 Levels of Lead and Demographic Covariates in U.S. Populations
The National Center for Health Statistics has provided the best currently available pic-
ture of blood lead levels among United States residents as part of the second National Health
and Nutrition Examination Study (NHANES II) conducted from February, 1976 to February, 1980
(Mahaffey et al., 1980; McDowell et al., 1981; Annest et al., 1982). The national estimates
are based on 9933 persons whose blood lead levels ranged from, 2.0 to 66.0 pg/dl. The median
blood lead for the entire U.S. population is 13.0 pg/dl.
Age appears to be one of the most important demographic covariates of blood lead levels.
Blood lead levels in children are generally higher than those in non-occupationally exposed
adults. Chlldred aged 24-36 months tend to have the highest blood lead levels. The age
trends in blood lead levels for children under 10 years old, as seen 1n three studies are pre-
sented in Figure 1-13. Blood l.ead levels in non-occupationally exposed adults may Increase
slightly with age due to skeletal lead accumulation.
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40
I I
i
it
10
J L
IDAHO STUDV
NEW YORK SCREEN IN8 . BLACKS
NEW YORK SCREENING • WHITES
NEW YORK SCREENING HISPANIC#
NHANfS II STUDY SLACKS
NHANES II STUDY • WHITES
I I I I
10
AGE IN YEARS
Figure 1-13. Geometric mean blood iMd levels by race and age for younger children
in the NHANES II study, and the Ksllogg/Silver Valley and New York Childhood
Screening Studies.
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Sex has a differential impact on blood lead levels depending on age. No significant dif-
ference exists between males and females less than seven years of age. Males above the age of
seven generally have higher blood lead levels than females. Race also plays a role, in that
blacks have higher blood lead levels than either whites or Hispanlcs. The reason for this has
yet to be totally disentangled from exposure.
Blood lead levels also seem to Increase with degree of urbanization. Data from NHANES II
show that blood lead levels in the United States, averaged from 1976 to 1980, increase from a
geometric mean of 11.9 ugAH in rural populations to 12.8 jjg/dl in urban populations less than
one million and increase again to 14.0 vg/dl 1n urban populations of one million or more,
(see Table 1-9).
Recent U.S. blood lead levels show that a downward has trend occurred consistently across
race, age, and geographic location. The downward pattern commenced in the early part of the
1970's and has continued into 1980. The downward trend has occurred from a shift in the en-
tire distribution and not just via a truncation in high blood lead levels. This consistency
suggests a general causative factor and attempts have been made to identify the causative
element. Reduction in lead emitted from the combustion of leaded gasoline is a prime candi-
date, but as yet no causal relationship has been definitively established.
Blood lead data from the NHANES II study demonstrates well, on a nationwide basis, a sig-
nificant downward trend over time (Annest et al., 1982). Mean blood lead levels dropped from
15.8 pg/dl during the first six months of the survey to 10.0 pg/dl during the last six months.
Mean values from these national data presented in six months increments from February 1976 to
February 1980 are displayed in Figure 1-14.
Blllick and colleagues have analyzed the results of blood lead screening programs con-
ducted by the City of New York. Geometric mean blood lead levels decreased for all three
racial groups and for almost all age groups in the period 1970-76. Figure 1-15 shows that the
downward trend covers the entire range of the frequency distribution of blood lead levels.
The decline in blood lead levels showed seasonal variability, but the decrease In time was
consistent for each season.
Gause et al. (1977) present data from Newark, New Jersey, which reinforces the findings
of Blllick and coworkers. Gause et al. studied the levels of blood lead among 5- and 6-year-
old children tested by the Newark Board of Education during the academic years 1973-74, 1974-
75, and 1975-76. Blood lead levels declined markedly during this 3-year period.
Rablnowitz and Needleman (1982) report a more recent study of umbilical cord blood lead
levels from 11,837 births between April, 1979 and April, 1981 in the Boston area. The overall
mean blood lead concentration was S.56 ± 3.19 (standard deviation) with a range from 0.0 to
37.9 jjg/dl. A downward trend 1n umbilical cord blood lead levels was noted over th.e two years
of the study.
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TABLE 1-9. WEIGHTED GEOMETRIC MEAN BLOOD LEAD LEVELS
FROM NHANES II SURVEY BY DEGREE OF URBANIZATION OF PLACE OF
RESIDENCE IN THE U.S. BY AGE AND RACE, UNITED STATES 1976-80
Degree of urbanization
Race and age
Urban,
£1 million
Urban,
<1 million
Rural
All races
Geometri c
mean (|jg/dl)
All ages
14.0
12.8
11.9
6 months-5 years
16.8
15.3
13.1
6-17 years
13.1
11.7
10.7
18-74 years
14.1
12.9
12.2
Whites
All ages
14.0
12.5
11.7
6' months-5 years
15.6
14.4
12.7
6-17 years
12.7
11.4
10.5
18-74 years
14.3
12.7
12.1
81acks
All ages
14.4
14.7
14.4
6 months-5 years
20.9
19.3
16.4
6-17 years
14.6
13.6
12.9
18-74 years
13.9
14.7
14.9
Source: Annest et. al., 1982.
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WINTER 1976
(FEB.)
WINTER 1977
(FEB.)
WINTER 1978 FALL 1978 WINTER 1979
(FEB.)
WINTER 1980
(FEB.)
(OCT.)
(FEB.)
0
10
5
15
20
25
30
36
40
46
60
66
CHRONOLOGICAL ORDER, 1 unit - 28 days
Figure 1-14. Average blood lead levels of U.S. population 6 months—74 years'. United States,
February 1976—February 1980, based on dates of examination of NHANES II examinees with
blood lead determinations.
Source: An nest et al. (1983).
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PRELIMINARY DRAFT
CHICAGO
NEW YORK
I
8
1
a
Z
o
g 10 —
o
1970 1171 1912 1973 1974 197B 197* 1977 1979 1979 1980
YEAR (Bsginning Jan. 1)
Figure 1-16. Time dependence of blood lead for blacks, aged 24 to 35
months. In New York City and Chicago,
Source; Adapted from Billick (19821.
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The importance of the distributional form of blood lead levels is that the distributional
form determines which measure of central tendency (arithmetic mean, geometric mean, median) is
most appropriate. It is even more important in estimating percentiles in the tail of the dis-
tribution, which represents those individuals at highest risk exposure-wise.
Based on the examination of the NHANES II data, as well as the results of several other
papers, it appears that the lognonnal distribution is the most appropriate for describing the
distribution of blood lead levels in homogeneous populations with nearly constant external
exposure levels. The lognonnal distribution appears to fit well across the entire range of the
distribution, including the right tail of the distribution. Blood lead levels, examined on a
population basis, have similarly skewed distributions. Blood lead levels from a population
thought to be homogenous 1n terms of demographic and lead exposure characteristics approxi-
mately follow a lognormal distribution. The geometric standard deviation for four different
studies are shown in Table 1-10. The values, including analytic error, are about 1.4 for
children and possibly somewhat smaller for adults. This allows an estimation of the upper
tail of the blood lead distribution, the group at higher risk.
Results obtained from the NHANES II study show that urban children generally have the
highest blood lead levels of any non-occupationally exposed population group. Furthermore,
black urban children have significantly higher blood lead levels than white urban children.
Several case control studies of children have shown that blood lead levels are related to hand
lead levels, house dust levels, lead in outside soil, interior paint lead level, and history
of pica. These factors are discussed in greater detail in the following sections.
1.11.2 Blood Lead vs. Inhaled Air Lead Relationships
The mass of data on the relationship of blood lead level and air lead exposure is compli-
cated by the need for reconciling the results of experimental and observational studies.
Further, the process of determining the best form of the statistical relationship deduced is
problematic due to the lack of consistency of range of the air lead expsoures encountered in
the various studies.
Because the main purpose of this document 1s to examine relationships of lead in air and
lead in blood under ambient conditions, EPA has chosen to emphasize the results of studies
most appropriately addressing this issue. A summary of the most appropriate studies appears
in Table 1-11. At air lead exposures of 3 pg/m3 or less, there is no statistically signifi-
cant difference between curvilinear and linear blood lead inhalation relationships. At air
lead exposures of 10 pg/m3 or more either nonlinear or linear relationships can be fitted.
Thus a reasonably consistent picture emerges in which the blood lead-air lead relationship by
direct inhalation was approximately linear in the range of normal ambient exposures (0.1 -
2.0 pg/m3.) Therefore EPA has fitted linear relationships to blood lead levels in the studies
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TABLE 1-10. SUMMARY OF POOLED GEOMETRIC STANDARD
DEVIATIONS AND ESTIMATED ANALYTIC ERRORS
Study
Pooled Geometric
Standard Deviations
Estimated
Inner City
Black Children
Inner City
White Children
Adult
Females
Adult
Males
Analytic
Error
NHANES II
1.37
1.39
1.36a
1.40a
0.021
N.Y. Childhood
Screening Study
1.41
1.42
-
-
(b)
Tepper- Levin
-
-
1.30
-
0.056C
Azar et al.
-
-
-
1.29
0.042C
Note: To calculate an estimated person-to-person GSD, compute Exp [(ln(GSD))2 -
j,
Analytic Error)1].
apoo1ed across areas of differing urbanization.
''not known, assumed to be similar to NHANES II.
ctaken from Lucas (1981).
to be described with the explicit understanding that the fitted relationships are intended
only to describe changes 1n blood due to modest changes in air lead among Individuals whose
blood lead levels do not exceed 30 jjg/dl.
The blood-lead inhalation slope estimates vary appreciably from one subject to another in
experimental and clinical studies, and from one study to another. The weighted slope and stan-
dard error estimates from the Griffin study (1.75 ± 0.35) were combined with those calculated
similarly for the Rabinowitz study in (2.14 1 0.47) and the Kehoe study in Table 11-20 (1.25 ±
0.35 setting DH = 0), yielding a pooled weighted slope estimate of 1.64 l 0.22 ijgAn per pg/m3
There are some advantages 1n using these experimental studies on adult males, but certain
deficiencies are acknowledged. The Kehoe study exposed subjects to a wide range of exposure
levels while in the exposure chamber, but did not control air lead exposures outside the
chamber. The Griffin study provided reasonable control of air lead exposure during the exper-
iment, but difficulties in defining the non-inhalation baseline for blood lead (especially in
the important experiment dt 3 pg/m3) add much uncertainty to the estimate. The Rabinowitz
stucjy controlled well for diet and other factors and, since they used stable lead isotope
tracers, they had no baseline problem. However, the actual air lead exposure of these
subjects outside the metabolic ward was not well determined.
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TABLE 1-11.
SUMMARY Of BLOOD INHALATION SLOPES (p)
pg/dl per pg/m3
Population
Study
Study
Type
N
Slope
Model Sensitivity*
of Slope
Children
Angle and Mclntire
(1979) Omaha, NE
Population
1074
1.92
(1.40-4.40)1*2'3
Roels et al. (1980)
Belgium
Population
148
2.46
(1.55-2.46)1,2
Yankel et al. (1977);
Walter et al. (1980)
Idaho
Populati on
879
1.52
(1.07-1.52)1,2'3
Adult
Male
Azar et al. (1975).
Five groups
Population
149
1.32
(1.08-1.59)2,3
Griffin et al.
(1975) NY
prisoners
Experiment
43
1.75
(1.52-3.38)4
Gross
(1979)
Experiment
6
1.25
(1.25-1.55)2
Rablnowitz et al.
(1973, 1976, 1977)
Experiment
5
2.14
(2.14-3.51)5
^Selected fro* among the mast plausible statistically equivalent models. For nonlinear
models, slope at 1.0 pg/m .
Sensitive to choice of other correlated predictors such as dust and soil lead.
2
Sensitive to linear vs. nonlinear at low air lead.
3
Sensitive to age as a covariate.
4
Sensitive to baseline changes in controls.
Sensitive to assumed air lead exposure.
Among population studies, only the Azar study provides a slope estimate in which indivi-
dual air lead exposures are known. However, there was no control of dietary lead intake or
other factors that affect blood lead levels, and slope estimates assuming only air lead and
location as covariables (1.32 ± 0.38) are not significantly different from the pooled experi-
mental studies.
There are no experimental inhalation studies on adult females or on children. The Inha-
lation slope for women should be roughly the same as that for men, assuming proportionally
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smaller air Intake and blood volume. The assumption of proportional size is less plausible
for children. Slope estimates for children from population studies are used 1n which some
other Important covariates of lead absorption were controlled or measured, e.g., age, sex,
dust exposure in the environment or on the hands. Inhalation slopes were estimated for the
studies of Angle and Hclntire (1.92 * 0.60), Roels (2.46 ± 0.58), and Yankel et al. (1.53 ±
0.064). The standard error of the Yankel study 1s extremely low and a weighted pooled slope
estimate for children would reflect essentially that study alone. In this case the small
standard error estimate is attributable to the very large range of air lead exposures of chil-
3
dren in the Silver Valley (up to 22 pg/m ). The relationship is in fact not linear, but in-
creases more rapidly In the upper range of air lead exposures. The slope estimate at lower
air lead concentrations may not wholly reflect uncertainty about the shape of the curve at
higher concentrations. The unweighted mean slope of the three studies and its standard error
estimate are 1.97 ± 0.39.
To summarize the situation briefly; (1) The experimental studies at lower air lead
levels (3.2 pg/m3 or less) and lower blood levels (typically 30 pg/dl or less) have linear
blood lead inhalation relationships with slopes p.| of 0-3.6 for most subjects. A typical
value of 1.64 ± 0.22 may be assumed for adults. (2) Population cross-sectional studies at
lower air lead and blood lead levels are approximately linear with slopes $ of 0.8-2.0. (3)
Cross-sectional studies 1n occupational exposure situations in which air lead levels are
J
higher (much above 10 pg/m ) and blood lead levels are higher (above 40 pfl/dl) show a much
more shallow linear blood lead inhalation relation. The slope p is in the range of 0.03-0.2.
(4) Cross-sectional and experimental studies at levels of air lead somewhat above the higher
3
ambient exposures (9-36 pg/m ) and blood leads of 30-40 pg/dl can be described either by
a nonlinear relationship with decreasing slope or by a linear relationship with intermediate
slope, approximately p = 0.5. Several biological mechanisms for these differences have been
discussed (Hammond et al., 1981; O'Flaherty et al., 1982; Chamberlain, 1983; Chamberlain and
Heard, 1981). Since no explanation for the decrease in steepness of the blood lead Inhalation
response to higher air lead levels has been generally accepted at this time, there is little
basis on which to select an interpolation formula from low air lead to high air lead expo-
sures. The increased steepness of the inhalation curve for the Kellogg/Silver Valley study is
inconsistent with the other studies presented. It may be that smelter situations are unique
and must be analyzed differently, or 1t may be that the curvatuve is the result of imprecise
exposure estimates. (5) The blood-lead Inhalation slope for children is at least as steep as
that for adults, with an estimate of 1.97 * 0.39 from three major studies. These slope esti-
mates are based on the assumption that an equilibrium level of blood lead is achieved within a
few months after exposure begins. This is only approximately true, since lead stored 1n the
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skeleton may return to blood after some years. Chamberlain et al. (1978) suggest that long
term Inhalation slopes should be about 30 percent larger than these estimates. Inhalation
slopes quoted here are associated with a half-life of blood lead in adults of about 30 days.
0'Flaherty et al. (1982) suggest that the blood-lead half-life may increase slightly with
duration of exposure, but this has not been confirmed (Kang et al., 1983).
Other studies, reviews, and analyses of the study are discussed in Section 11.4, to which
the reader 1s referred for a detailed discussion and for a review of the key studies and their
analyses.
It aust not be assumed that the direct inhalation of air lead is the only air lead con-
tribution that needs to be considered. Smelter studies allow partial assessment of the air
lead contributions to soil, dust, and finger lead. Useful ecological models to study the pos-
sible propagation of lead through the food chain have not yet been developed. The direct In-
halation relationship does provide useful information on changes in blood lead as responses to
changes in air lead on a time scale of several months. The indirect pathways through dust and
soil and through the food chain may thus delay the total blood lead response to changes in air
lead, perhaps by one or more years.
1.11.3 Dietary Lead Exposures Including Mater
Dietary absorption of lead varies greatly from one person to another and depends on the
physical and chemical form of the carrier, on nutritional status, and on whether lead is in-
gested with food or between meals. These distinctions are particularly important for con-
sumption of leaded paint, dust, and soil by children. Typical values of 10 percent absorption
of Ingested lead into blood have been assumed for adults and 25-50 percent for children.
It is difficult to obtain accurate dose-response relationships between blood lead levels
and lead level in food or water. Dietary intake must be estimated by duplicate diets or fecal
lead determinations. Water lead levels can be determined with some accuracy, but the varying
amounts of water consumed by different individuals adds to the uncertainty of the estimated
relationships.
Quantitative analyses relating blood lead levels and dietary lead exposures have been re-
ported. Studies on infants provide estimates that are in close agreement. Only one indivi-
dual study is available for adults; another estimate from a number of pooled studies is also
available. These two estimates are 1n good agreement. Most of the subjects in the Sherlock
et al. (1982) and United Kingdom Central Directorate on Environmental Pollution (1982) studies
received quite high dietary lead levels (>300 pg/day). The fitted cube root equations give
high slopes at lower dietary lead levels. On the other hand, the linear slope of the United
Kingdom Central Directorate on Environmental Pollution (1982) study 1s probably an underesti-
mate of the slope at lower dietary lead levels. For these reasons, the Ryu et al. (1983)
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study 1s the most believable, although It only applies to infants. Estimates for adults
should be taken from the experimental studies or calculated from assumed absorption and half-
life values.
Host of the dietary intake supplements were so high that many of the subjects had blood
lead concentrations much in excess of 30 pg for a considerable part of the experiment. Blood
lead levels thus may not completely reflect lead exposure, due to the previously noted non-
linearity of blood lead response at high exposures. The slope estimates for adult dietary in-
take are about 0.02 pg/dl increase 1n blood lead per pg/d Intake, but consideration of blood
lead kinetics may increase this value to about 0.04 pg/dl per pg/d intake. Such values are
somewhat (about 0.05 pg/dl per pd/d) lower than those estimated from the population studies
extrapolated to typical dietary intakes. The value for infants is much larger. The relation-
ship between blood lead and water lead is not clearly defined and 1s often described as non-
linear. Water lead intake varies greatly from one person to another. It has been assumed
that children can absorb 25 to 50 percent of lead in water. Many authors chose to fit cube
root models to their data, although polynomial and logarithmic models were also used. Unfor-
tunately, the form of the model greatly influences the estimated contributions to blood lead
levels from relatively low water lead concentrations.
Although there is close agreement in quantitative analyses of relationships between blood
lead levels and dietary lead concentrations, there 1s a larger degree of variability in
results of the various water lead studies. The relationship is curvilinear but Its exact for*
1s yet to be determined. At typical levels for U.S. populations the relationship appears to
be linear. The only study that determines the relationship based on lower water lead values
(<100 pg/1) is the Pocock et al. (1983) study. The data from this study, as well as the
authors themselves, suggest that the relationship 1s linear for this lower range of water lead
levels. Furthermore, the estimated contributions to blood lead levels from this study are
quite consistent with the polynomial models from other studies. For these reasons, the Pocock
et al. (1983) slope of 0.06 is considered to represent the best estimate. The possibility
still exists, however, that the higher estimates of the other studies may be correct in cer-
tain situations, especially at higher water lead levels (>100 pg/1).
1.11.4 Studies Relating Lead in Soil and Dust to Blood Lead
The relationship of exposure to lead contained in soil and house dust and the amount of
lead absorbed by humans, particularly children, has been the subject of a number of scientific
investigations. Some of these studies have been concerned with the effects of exposures
resulting from the ingestion of lead 1n dust (Ouggan and Williams, 1977; Barltrop, 1975;
Creason et al., 1975); others have concentrated on the means by which the lead in soil and
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dust becomes available to the body (Sayre et al., 1974). Sayre et al. (1974) demonstrated the
feasibility of house dust as a source of lead for children in Rochester, NY. Two groups of
houses, one inner city and the other suburban, were chosen for the study. Lead-free sanitary
paper towels were used to collect dust samples from house surfaces and the hands of children
(Vostal et al., 1974). The medians for the hand and household samples were used as the cut-
points in the chi-square contingency analysis. A statistically significant difference between
the urban and suburban homes for dust levels was noted, as was a relationship between house-
hold dust levels and hand dust levels (Lepow et al., 1975).
Studies relating soil lead to blood lead levels are difficult to compare. The relation-
ship obviously depends on depth of soil lead, age of the children, sampling method, cleanli-
ness of the home, mouthing activities of the children, and possibly many other factors. Vari-
ous soil sampling methods and sampling depths have been used over time; as such they may not
be directly comparable and may produce a dilution effect of the major lead concentration con-
tribution from dust, which is located primarily in the top 2 cm of the soil.
Increases in soil dust lead significantly increase blood lead in children. From several
studies EPA estimates an increase of 0.6 to 6.8 Mfl/dl in blood lead for each Increase of 1000
ng/g in soil lead concentration. The values from the Stark et al. (1982) study may represent
a reasonable median estimate, i.e. about 2.0 pg/dl for each 1000 pg/dl Increase in soil lead.
Household dust also Increases blood lead, children from the cleanest homes in the Kellogg/
Silver Valley Study having 6 pg/dl less lead in blood, on average, than those from the house-
holds with the most dust.
1.11.5 Paint Lead Exposures
A major source of environmental lead exposure for many members of the general population
comes from lead contained in both interior and exterior paint on dwellings. The amount of
lead present, as well as Its accessibility, depends upon the age of the residence (because
older buildings contain paint manufactured before lead content was regulated) and the physical
condition of the paint. In a survey of lead levels 1n 2370 randomly selected dwellings 1n
Pittsburgh, PA (Shier and Hall, 1977), paint with high levels of lead were most frequently
found in pre-1940 residences. One cannot assume, however, that high level lead paint is
absent in dwellings built after 1940. In the case of the houses surveyed in Pittsburgh, about
20 percent of the residences built after 1960 have at least one surface with more than 1.5
mg/cm lead. In fiscal year 1981, the U.S. Centers for Disease Control (1982), screened
535,730 children and found 21,897 with lead toxicity. Of these cases, 15,472 dwellings were
inspected and 10,666 (approximately 67 percent) were found to have leaded paint.
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1.11.6 Specific Source Studies
Two field investigations have attempted to derive an estiaiate of the amount of lead from
gasoline that is absorbed by the blood of individuals. Both of these investigations used the
fact that the isotopes of lead are stable and thus, the varying proportions of the isotopes
present in blood and environmental samples can indicate the source of the lead. The Isotope
Lead Experiment (ILE) is a massive study that attempted to utilize differing proportions of
the Isotopes in geologic formations to infer the proportion of lead in gasoline that is
absorbed by the body. The other study utilized existing natural shifts in isotopic pro-
portions in an attempt to do the sane thing.
The ILE is a large scale community trial in which the geologic source of lead for
antiknock compounds in gasoline was manipulated to change the Isotopic composition of lead 1n
the atmosphere (Garibaldi et al., 1975; Facchetti, 1979). The isotopic lead ratios obtained
in the samples analyzed are displayed in Figure 1-16. It can be easily seen that the airborne
particulate lead rapidly changed its isotope ratio in line with expectation. Ratios in the
blood samples appeared to lag somewhat behind. Background lead isotopic ratios were 1.1603 ±
0.0028 in rural areas and 1.1609 ± 0.0015 in Turin In 1975. In Turin school children in
1977-78, a mean isotopic ratio of 1.1347 was obtained.
Preliminary analysis of the isotope ratios in air lead has allowed the estimation of the
fractional contribution of gasoline in the city of Turin, in small communities within 25 km of
Turin and in small communities beyond 25 km (Facchetti and Geiss, 1982). At the time of maxi-
mal use of Australian lead isotope in gasoline (1978-79), about 87.3 percent of the air lead
in Turin and 58.7 percent of the air lead in the countryside was attributable to gasoline. The
determination of lead isotope ratios was essentially independent of specific air lead concen-
trations. During that time, air lead averaged about 2.0 m9/«3 in Turin (from 0.88 to 4.54
% <3
)ifl/« depending on location of the sampling site), about 0.56 vq/m in the nearby communities
3 3
(0.30 to 0.67 jjg/m ), and about 0.30 yg/m in distant locations.
Isotope ratios in the blood of 35 subjects also changed, and the fraction of lead in
blood attributable to gasoline could be estimated Independently of blood level concentration.
The mean fraction decreased from 23.7 ± 5.4 percent in Turin to 12.5 ± 7,1 percent in the
nearby countryside, and to 11.0 ± 5.8 percent in the remote countryside.
These results can be combined with the actual blood lead concentrations to estimate the
fraction of the gasoline uptake that is attributable to direct inhalation and that which is
not. The results are shown in Table 1-12 (based on a suggestion by Dr. Fachetti). As con-
cluded earlier, an assumed value of p=l.6 is plausible for predicting the amount of lead ab-
3
sorbed into blood at air lead concentrations less than 2.0 pg/m . The predicted values for
airborne lead derived from leaded gasoline range from 0.28 to 2.79 in blood due to
direct inhalation. The total contribution of blood lead from gasoline is much larger, from
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I I I I I I I I I I I I I I I I I
*) BASED ON A LIMITED NUMBER OF SAMPLES
- Pb 206/Pb 207
• ADULTS <25 km
BLOOD A ADULTS > 25 km
O ADULTS TURIN
~ TRAFFIC WARDENS-TURIN
¦ SCHOOL CHILDREN-TURIN
1.20
1.18
1.18
1.14
1.12
1.10
1.08
1.08
AIRBORNE
PARTICULATE
• TURIN
A COUNTRYSIDE
O PETROL
Phase 0
Phase 1
Phase 2
Ptiasa 3
I H I 1 H I H 1 I 1 I I I I
74
75
7#
77
79
79
80
81
Rgure 1-16. Change in Pb-206/Pb-207 ratios in petrol, airborne particulate,
and blood from 1974 to 1981.
Source: Facchetti and Geiss (19821.
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TABLE 1-12. ESTIMATED CONTRIBUTION OF LEADED GASOLINE TO BLOOD LEAO
BY INHALATION ANO NON-INHALATION PATHWAYS
Air Lead
Lead
Mean
Blood
Lead
Non-
Estimated
Fraction
Air
Fraction
Blood
Lead
From
Inhaled
Fraction
From
Lead h
From
Lead A
From
Gasoline
In Air
Lead From
Gas-Lead h
Gaso-
Cone.
Gaso-
Cone.
Gaso-
line
Gaso-
line9
Inhalation
Locatlon line
line
(Mfl/m3)
(MS/dl)
(M9/dl)
(Mg/di)
(lig/dl)
Turin 0.873 2.0 0.237 21.77 5.16 2.79 2.37 0.54
<25 km 0.587 0.56 0.125 25.06 3.13 0.53 2.60 0.17
>25 km 0.587 0.30 0.110 31.78 3.50 0.28 3.22 0.08
aFraction of air lead in Phase 2 attributable to lead In gasoline.
'Wan air lead In Phase 2, pg/nA
°Mean fraction of blood lead 1n Phase 2 attributable to lead in gasoline.
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In summary, the direct Inhalation pathway accounts for only a fraction of the total air
lead concentration of blood, the direct inhalation contribution being on the order of 12-23
percent of the total uptake of lead attributable to gasoline, using Stephen's assumptions.
This is consistent with estimates from the ILE study.
Another approach was taken in New York City. BilHck et al. (1979) presented several
possible explanations for observed declines in blood lead levels (discussed earlier above) and
evidence supporting and refuting each. The suggested contributing factors were the active
educational and screening program of the New York City Bureau of Lead Poisoning Control, and
the decrease in the amount of lead-based paint exposure as a result of rehabilitation or
removal of older housing stock of changes in environmental lead exposure. Information was
available only to partially evaluate the last source of lead exposure and particularly only
for ambient air lead levels. Air lead measurements were available during the entire study
period for only one station which was located on the west side of Manhattan at a height of
56 m. Superimposition of the air lead and blood lead levels indicated a similarity in both
upward cycle and decline. The authors cautioned against overinterpretation by assuming that
one air monitoring site was representative of the air lead exposure of New York City resi-
dents. With this in mind, the investigators fitted a multiple regression model to the data to
try to define the important determinants of blood lead levels for this population. Age, eth-
nic group and air lead level were all found to be significant determinants of blood lead
levels. The authors further point out the possibility of a change in the nature of the popu-
lation being screened before and after 1973. They reran this regression analysis separately
for years both before and after 1973. The same results were still obtained, although the
exact coefficients derived varied.
BilHck et al. (1980) extended their previous analysis of the data from the single moni-
toring site mentioned earlier. The investigators examined the possible relationship between
blood lead level and the amount of lead in gasoline used in the New York City area. Figures
1-17 and 1-18 present illustrative trend lines in blood leads for blacks and Hispanics and air
lead and gasoline lead, respectively. Several different measures of gasoline lead were used:
(1) mid-Atlantic Coast (NY, NJ, Conn); (2) New York City plus New Jersey, and (3) New York
city plus Connecticut. The lead in gasoline trend line appears to fit the blood lead trend
line better than the air lead trend, especially in the summer of 1973.
1.11.7 Primary Smelters Populations
In 1972, the Centers for Disease Control studied the relationships between blood lead
levels and environmental factors in the vicinity of a primary smelter emitting lead, copper,
and zinc located in El Paso, Texas, that had been 1n operation since the late 1800's
(Landrigan et al., 1975; U.S. Centers for Disease Control, 1973). Daily high volume samples
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QUARTERLY SAMPLING DATE
Figure 1-17. Geometric mean blood lead levels of New York City
children (aged 25-38 months) by ethnic group, and ambient air lead
concentration versus quarterly sampling period, 1970-1976.
Source: Billick et al. (1980).
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Figure 1-18. Geometric maan blood lead levels of New York City
children (aged 25-38 months) by ethnic group, and estimated
amount of lead present in gasoline sold in New York, New Jersey,
and Connecticut versus quarterly sampling period, 1970-1976.
Source: Billick et al. (1980).
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3
collected on 86 days between February and June, 1972 averaged 6.6 jjg/m . These air lead
levels fell off rapidly with distance, reaching background values approximately 5 km from the
smelter. Levels were higher downwind, however. High concentrations of lead in soil and house
dusts were found, with the highest levels occurring near the smelter. The geometric means of
lead content in 82 soil and 106 dust samples from the sector closest to the smelter were 1791
and 4022 pg/g, respectively. Geometric means of both soil and dust lead levels near the
smelter were significantly higher than those in study sectors 2 or 3 km farther away. Sixty-
nine percent of children 1- to 4-years old living near the smelter had blood lead levels <40
pg/dl, and 14 percent had blood lead levels that exceeded 60 pg/dl. Concentrations in older
individuals were lower; nevertheless, 45 percent of the children 5- to 9-years old, 31 percent
of the individuals 10- to 19-years old, and 16 percent of the individuals above age 19 had
blood lead levels exceeding 40 pg/dl.
Cavalleri et al. (1981) studied children in the vicinity of a lead smelter and children
from a control area (4 km from the smelter). Since the smelter had installed filters 8 years
before the study, the older children living in the smelter area had a much higher lifetime
exposure. A striking difference in blood lead levels of the exposed and control populations
was observed; levels in the exposed population were almost twice that in the control popula-
tion. The geometric mean for nursery school children was 15.9 and 8.2 pg/dl for exposed and
control, respectively. For primary school it was 16.1 and 7.0 pg/dl. The air lead levels
3 3
were between 2 to 3 pg/m in the exposed and 0.56 pg/m in the control cases.
1.11.8 Secondary Exposure of Children
Excessive intake and absorption of lead on the part of children can result when parents
who work 1n a dusty environment with a high lead content bring dust home on their clothing,
their shoes, or even their automobiles. Once home, their children are exposed to the high-
lead content dust.
Landrigan et al. (1976) reported that the 174 children of smelter workers who live within
24 km of a smelter had significantly higher blood lead levels (a mean of 55.1 pg/dl) than 511
children of persons in other occupations who lived in the same areas (whose mean blood lead
levels were 43.7 pg/dl). Other studies have documented increased lead absorption in children
of families where at least one member was occupationally exposed to lead (Fischbein et al.,
1980a). The occupational exposures often involved battery plant operations (Norton et al.,
1982; U.S. Centers for Disease Control, 1977; Dolcourt et al., 1978, 1981; Watson et al.,
1978; Ferguson et al., 1981), as well as other occupations (Snee, 1982b; Rice et al., 1978).
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1.12 BIOLOGICAL EFFECTS OF LEAD EXPOSURE
1.12.1 Introduction
Lead has diverse biological effects 1n humans and animals. Its effects are seen at the
subcellular level of organellar structures and processes as well as at the overall level of
general functioning that encompasses all systems of the body operating in a coordinated, in-
terdependent fashion.
This review seeks not only to categorize and describe the various biological effects of
lead but to identify the exposure levels at which such effects occur and the mechanisms under-
lying then. The dose-response curve for the entire range of lead's biological effects 1s
rather broad, with certain biochemical changes occurring at relatively low levels of expo-
sure and perturbations in some organ systems, such as the endocrine, being obvious only at
relatively high exposure levels. In terms of relative vulnerability to lead's deleterious
effects, the developing organism appears to be more sensitive than the mature individual,
particularly where the neurotoxic effects of lead are concerned.
1.12.2 Subcellular Effects of Lead
The biological basis of lead toxicity is its ability to bind to 11gating groups in bio-
molecular substances crucial to various physiological functions, thereby interfering with
these functions by, for example, competing with native essential metals for binding sites,
inhibiting enzyme activity, and inhibiting or otherwise altering essential ion transport.
These effects are modulated by: (1) the inherent stability of such binding sites for lead;
(2) the compartmental1zation kinetics governing lead distribution among body compartments,
among tissues, and within cells; and (3) the differences in biochemical organization across
cells and tissues due to their specific functions. Given the complexities introduced by items
2 and 3, it is not surprising that no single, unifying mechanism of lead toxicity across all
tissues in humans and experimental animals has yet been identified.
In so far as effects of lead on activity of various enzymes are concerned, many of the
available studies concern _in vitro behavior of relatively pure enzymes with marginal relevance
to various effects in vivo. On the other hand, certain enzymes are basic to the effects of
lead at the organ or organ system level, and discussion is best reserved for such effects in
sections below dealing with particular organ systems. This section is mainly concerned with
organellar effects of lead, particularly those which provide some rationale for lead toxicity
at higher levels of biological organization. Particular emphasis is placed on the mitochon-
drion, since this organelle is not only affected by lead 1n a number of ways but has provided
the most data.
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The main target organelle for lead toxicity in a variety of cell and tissue types clearly
is the mitochondrion, followed probably by cellular and intracellular membranes. The iiito-
chondrlal effects take the form of structural changes and marked disturbances in mitochondrial
function within the cell, particularly in energy metabolism and ion transport. These effects
in turn are associated with demonstrable accumulation of lead in mitochondria, both in vivo
and in vitro. Structural changes include mitochondrial swelling in a variety of cell types as
well as distortion and loss of cristae, which may occur at relatively moderate levels of lead
exposure. Similar changes have also been documented in lead workers across a range of ex-
posure levels.
Uncoupled energy metabolism, inhibited cellular respiration using both succinate and
nicotinamide adenine dinucleotide (NAD)-linked substrates, and altered kinetics of intracellu-
lar calcium have been demonstrated in vivo using mitochondria of brain and non-neural tissue.
In some cases, the lead exposure level associated with such changes has been relatively moder-
ate. Studies documenting the relatively greater sensitivity of this organelle in young vs.
adult animals in terms of mitochondrial respiration have been reported. The cerebellum
appears to be particularly sensitive, providing a connection between mitochondrial impairment
and lead encephalopathy. Impairment by lead of mitochondrial function in the developing brain
has also been consistently associated with delayed brain development, as indexed by content of
various cytochromes. In the rat pup, ongoing lead exposure from birth is required for this
effect to be expressed, indicating that such exposure must occur before, and is inhibitory to,
the burst of oxidative metabolism activity that occurs in the young rat at 10 through 21 days
postnatally.
In vivo lead exposure of adult rats has also been seen to markedly inhibit cerebral cor-
tex intracellular calcium turnover in a cellular compartment that appears to be the mitochon-
drion. The effect was seen at a brain lead level of 0.4 ppm. These results are consistent
with a separate study showing increased retention of calcium in the brain of lead-dosed guinea
pigs. A number of reports have described the j_n vivo accumulation of lead in mitochondria of
kidney, liver, spleen, and brain tissue, with one study showing that such uptake was slightly
more than occurred in the nucleus. These jiata are not only consistent with the various dele-
terious effects of lead on mitochondria but are also supported by other investigations in
vitro.
Significant decreases in mitochondrial respiration _in vitro using both NAD-linked and
succinate substrates have been observed for brain and non-neural tissue mitochondria in the
presence of lead at micromolar levels. There appears to be substrate specificity in the inhi-
bition of respiration across different tissues, which may be a factor in differential organ
toxicity. Also, a number of enzymes involved in intermediary metabolism in isolated mitochon"
dria have been observed to undergo significant inhibition of activity with lead.
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A particular focus on lead's effects on isolated mitochondria has been ion transport,
especially with regard to calcium. Lead movement into brain and other tissue mitochondria
involves active transport, as does calcium. Recent sophisticated kinetic analyses of desat-
uration curves for radiolabeled lead or calcium indicate that there is striking overlap in the
cellular metabolism of calcium and lead. These studies not only establish the basis of lead's
easy entry into cells and cell compartments, but also provide a basis for lead's impairment of
intracellular ion transport, particularly in neural cell mitochondria, where the capacity for
calcium transport is 20-fold higher than even in heart mitochondria.
Lead is also selectively taken up in isolated mitochondria in vitro, including the mito-
chondria of synaptosomes and brain capillaries. Given the diverse and extensive evidence of
lead's impairment of mitochondrial structure and function as viewed from a subcellular level,
it is not surprising that these derangements are logically held to be the basis of dysfunction
of heme biosynthesis, erythropoiesis, and the central nervous system. Several key enzymes in
the heme biosynthetic pathway are intramitochondrial, particularly ferrochelatase. Hence, it
is. to be expected that entry of lead into mitochondria will impair overall heme biosynthesis,
and in fact this appears to be the case in the developing cerebellum. Furthermore, the levels
of lead exposure associated with entry of lead into mitochondria and expression of mitochon-
drial injury can be relatively moderate.
Lead exposure provokes a typical cellular reaction in human and other species that has
been morphologically characterized as a lead-containing nuclear inclusion body. While it has
been postulated that such inclusions constitute a cellular protection mechanism, such a
mechanism is an imperfect one. Other organelles, e.g., the mitochondrion, also take up lead
and sustain injury in the presence of inclusion formations. Chromosomal effects and other
indices of genotoxicity in humans and animals are considered in Section 1.12.7.
In theory, the cell membrane is the first organelle to encounter lead and it is not
surprising that cellular effects of lead can be ascribed to interactions at cellular and
intracellular membranes in the form of distrubed ion transport. The inhibition of membrane
(Na+,K+)-ATPase of erythrocytes as a factor in lead-impaired erythropoiesis is noted else-
where. Lead also appears to interfere with the normal processes of calcium transport across
membranes of different tissues. In peripheral cholinergic synaptosomes, lead is associated
with retarded release of acetylcholine owing to a blockade of calcium binding to the membrane,
while calcium accumulation within nerve endings can be ascribed to inhibition of membrane
(Na\K+)-ATPase.
Lysosomes accumulate in renal proximal convoluted tubule cells of rats and rabbits given
lead over a range of dosing. This also appears to occur in the kidneys of lead workers and
seems to represent a disturbance in normal lysosomal function, with the accumulation of
lysosomes being due to enhanced degradation of proteins because of the effects of lead else-
where within the cell.
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1.12.3. Effects of Lead on Heme Biosynthesis. Erythropoiesis, and Erythrocyte Physiology in
Humans and Animals
The effects of lead on heme biosynthesis are well known because of both their prominence
and the large number of studies of these effects in humans and experimental animals. The
process of heme biosynthesis starts with glycine and succinyl-coenzyme A, proceeds through
formation of protoporphyrin IX, and culminates with the insertion of divalent iron into the
porphyrin ring, thus forming heme. In addition to being a constituent of hemoglobin, heme is
the prosthetic group of a number of tissue hemoproteins having variable functions, such as
Rtyoglobin, the P-450 component of the mixed function oxygenase system, and the cytochromes of
cellular energetics. Hence, disturbance of heme biosynthesis by lead poses the potential for
multiple-organ toxicity.
At present, the steps 1n the heme synthesis pathway that have been best studied with re-
spect to lead's effects involve three enzymes: (1) stimulation of mitochondrial delta-amino-
levulinic acid synthetase (ALA-S), which mediates the formation of delta-aminolevulinic acid
(ALA); (2) direct inhibition of the cytosolic enzyme, delta-aminolevulinic acid dehydrase
(ALA-D), which catalyzes formation of porphobilinogen from two units of ALA; and (3) inhibi-
tion of the insertion of iron (II) into protoporphyrin IX to form heme, a process mediated by
the enzyme ferrochelatase.
Increased ALA-S activity has been documented in lead workers as well as lead-exposed ani-
mals, although the converse, an actual decrease in enzyme activity, has also been observed in
several experimental studies using different exposure methods. It would appear, then, that
enzyme activity increase via feedback derepression or that activity inhibition may depend on
the nature of the exposure. In an jn vitro study using rat liver cells in culture, ALA-S
activity could be stimulated at levels as low as 5.0 )jM or 1.0 |jg Pb/g preparation. In the
same study, increased activity was seen to be due to biosynthesis of more enzyme. The thres-
hold for lead stimulation of ALA-S activity in humans, based upon a study using leukocytes
from lead workers, appears to be about 40 m9 Pb/dl. The generality of this threshold level to
other tissues is dependent upon how well the sensitivity of leukocyte mitochondria mirrors
that in other systems. It would appear that the relative impact of ALA-S activity stimulation
on ALA accumulation at lower levels of lead exposure is considerably less than the effect of
ALA-D activity inhibition: at 40 Mfl/dl blood lead, ALA-D activity is significantly depressed,
whereas ALA-S activity only begins to be affected at that blood lead concentration.
Erythrocyte ALA-D activity is very sensitive to lead inhibition, which is reversed by re-
activation of the sulfhydryl group with agents such as dithiothreitol, zinc, or zinc plus glu-
tathione. The zinc levels employed to achieve reactivation, however, are well above normal
physiological levels. Although zinc appears to offset the inhibitory effects of lead observed
in human erythrocytes jn vitro and in animal studies, lead workers exposed to both zinc and
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lead do not show significant changes in the relationship of ALA-D activity to blood lead con-
centration when compared to workers exposed only to lead. In contrast, zinc deficiency in
animals has been shown to significantly Inhibit ALA-D activity, with concomitant accumulation
of ALA in urine. Since zinc deficiency has also been associated with increased lead absorp-
tion in experimental studies, the possibility exists for a dual effect of such deficiency on
ALA-D activity: (1) a direct effect on activity due to reduced zinc availability, as well as
(2) the effect of increased lead absorption leading to further inhibition of such activity.
The activity of erythrocyte ALA-D appears to be inhibited at virtually all blood lead
levels measured so far, and any threshold for this effect in either adults or children remains
to be determined. A further measure of this enzyme's sensitivity to lead comes from a report
noting that rat bone marrow suspensions show inhibition of ALA-D activity by lead at a level
of 0.1 pg/g suspension. Inhibition of ALA-D activity in erythrocytes apparently reflects a
similar effect in other tissues. Hepatic ALA-D activity was inversely correlated in lead
workers with both the erythrocyte activity as well as blood lead. Of significance are the ex-
perimental animal data showing that (1) brain ALA-D activity is inhibited with lead exposure
and (2) inhibition appears to occur to a greater extent in the brain of developing vs. adult
animals. This presumably reflects greater retention of lead in developing animals. In the
avian brain, cerebellar ALA-D activity is affected to a greater extent than that of the
cerebrum and, relative to lead concentration, shows inhibition approaching that occurring in
erythrocytes.
The inhibition of ALA-D activity by lead is reflected in increased levels of its sub-
strate, ALA, in blood, urine, and tissues. In one investigation, the increase in urinary ALA
was seen to be preceded by a rise in circulating levels of the metabolite. Blood ALA levels
were elevated at all corresponding blood lead values down to the lowest value determined (18
pg/dl), while urinary ALA was seen to rise exponentially with blood ALA. Urinary ALA has been
employed extensively as an indicator of excessive lead exposure in lead workers. The value of
this measurement for diagnostic purposes in pediatric screening, however, is limited if only
spot urine collection 1s done; more satisfactory data can be obtained in cases where 24-hour
collections are feasible. A large number of Independent studies have documented that there is
a direct correlation between blood lead and the logarithm of urinary ALA in adult humans and
children, and that the threshold is commonly accepted as being 40 pg/dl. Several studies of
.lead workers also Indicate that the correlation of urinary ALA with blood lead continues below
this value. Furthermore, one report has demonstrated that the slope of the dose-effect curve
in lead workers is dependent upon the level of exposure.
The health significance of lead-inhibited ALA-D activity and accumulation of ALA at low
levels of exposure has been an issue of some controversy. One view 1s that the "reserve
capacity" of ALA-D activity is such that only high accumulations of the enzyme's substrate,
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ALA, 1n accessible Indicator media would result in significant inhibition of activity. One
difficulty with this view is that it is not possible to quantify at lower levels of lead ex-
posure the relationship of urinary ALA to levels in target tissues nor to relate the potential
neurotoxicity of ALA at any level of build-up to levels in indicator media; i.e., the thres-
hold for potential neurotoxicity of ALA in terms of blood lead nay be different from the level
associated with urinary accumulation.
Accumulation of protoporphyrin in the erythrocytes of individuals with lead intoxication
has been recognized since the 1930s, but it has only recently been possible to quantitatively
assess the nature of this effect via the development of specific, sensitive micromethods of
analysis. Accumulation of protoporphyrin IX in erythrocytes is the result of Impaired place-
ment of iron (II) in the porphyrin moiety to form heme, an intramitochondrial process mediated
by the enzyme ferrochelatase. In lead exposure, the porphyrin acquires a zinc ion in lieu of
native iron, thus forming zinc protoporphyrin (ZPP), and is tightly bound in available heme
pockets for the life of the erythrocytes. This tight sequestration contrasts with the rela-
tively mobile non-metal, or free, erythrocyte protoporphyrin (FEP) accumulated in the congen-
ital disorder erythropoietic protoporphyria.
Elevation of erythrocyte ZPP has been extensively documented as being exponentially cor-
related with blood lead in children and adult lead workers and is presently considered one of
the best indicators of undue lead exposure. Accumulation of ZPP only occurs in erythrocytes
formed during lead's presence in erythroid tissue, resulting in a lag of at least several
weeks before such build-up can be measured. It has been shown that the level of such accumu-
lation in erythrocytes of newly-employed lead workers continues to increase when blood leae
has already reached a plateau. This would influence the relative correlation of ZPP and blood
lead in workers with a short exposure history. In individuals removed from occupational expo-
sure, the ZPP level in blood declines much more slowly than blood lead, even years after re-
moval from exposure or after a drop in blood lead. Hence, ZPP level would appear to be a more
reliable indicator of continuing intoxication from lead resorbed from bone.
The measurable threshold for the effect of lead on ZPP accumulation is affected by the
relative spread of blood lead and corresponding ZPP values measured. In young children (under
four years of age) the ZPP elevation typically associated with iron-deficiency anemia should
be taken into account. In adults, a number of studies Indicate that the threshold for ZPP
elevation with respect to blood lead is approximately 25-30 jifl/dl- In children 10-15 years
old the threshold is about 16 pg/dl; in this age group, iron deficiency is not a factor. In
one report, it was noted that children over four years of age showed the same threshold, 15.5
pg/dl, as a second group under four years old, Indicating that iron deficiency was not a
factor in the study. Fifty percent of the children were found to have significantly elevated
EP levels (2 standard deviations [SDs] above reference mean EP) or a dose-response threshold
level of 25 Mg/dl.
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Below 30-40 pig/d1, any assessment of the ZPP-blood lead relationship is strongly influ-
enced by the relative analytical proficiency for measurement of both blood lead and EP. The
types of statistical treatments given the data are also important. In a recent detailed sta-
tistical study involving 2004 children, 1852 of whom had blood lead values below 30 pg/dl.
segmental line and probit analysis techniques were employed to assess the dose-effect thres-
hold and dose-response relationship. An average blood lead threshold for the effect using
both statistical techniques yielded a value of 16,5 pg/dl for either the full group or those
subjects with blood lead levels below 30 Hfl/dl- The effect of iron deficiency was tested for
and removed. Of particular interest was the finding that the blood lead values corresponding
to EP elevations more than 1 or 2 standard deviations above the reference mean in 50 percent
of the children were 28.6 or 35.7 yg Pb/dl, respectively. Hence, fully half of the children
were seen to have significant elevations of EP at blood lead levels around the currently used
cut-off value for undue lead exposure, 30 ng/dl. From various reports, children and adult
fenales appear to be more sensitive to the effects of lead on EP accumulation at any given
blood lead level, with children being somewhat more sensitive than adult females.
Effects of lead on ZPP accumulation and reduced heme formation are not restricted to the
erythropoietic system. Recent studies show that reduction of serum 1,25-dihydroxy vitamin D
seen with even low level lead exposure is apparently the result of lead's inhibition of the
activity of renal 1-hydroxylase, a cytochrome P-450 mediated enzyme. Cytochrome P-450, a
heme-containing protein, is an integral part of the hepatic mixed function oxygenase system
and is known to be affected in humans and animals by lead exposure, particularly acute
intoxication. Reduced P-450 content has been found to be correlated with impaired activity of
such detoxifying enzyme systems as aniline hydroxylase and aminopyrine demethylase.
Studies of organotypic chick dorsal root ganglion in culture show that the nervous system
not only has heme biosynthetic capability but that such preparations elaborate porphyrinic ma-
terial in the presence of lead. In the neonatal rat, chronic exposure to lead resulting in
moderately elevated blood lead levels is associated with retarded growth in the hemoprotein
cytochrome C and with disturbed electron transport in the developing rat cerebral cortex.
These data parallel the effect of lead on AlA-D activity and ALA accumulation 1n neural
tissue. When both of these effects are viewed within the toxicokinetic context of increased
retention of lead in both developing animals and children, there is an obvious, serious
potential for impaired heme-based metabolic function in the nervous system of lead-exposed
children.
As can be seen from the above discussion, the health significance of ZPP accumulation
rests with the fact that such build-up is evidence of impaired heme and hemoprotein formation
in tissues, particularly the nervous system, arising from entry of lead into mitochondria.
Such evidence for reduced heme synthesis 1s consistent with a diverse body of data documenting
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lead-associated effects on mitochondria, including impairment of ferrochelatase activity. As
a mitochondrial enzyme, ferrochelatase activity may be inhibited either directly by lead or
indirectly by impairment of iron transport to the enzyme.
The relative value of the lead-ZPP relationship in erythropoietic tissue as an index of
this effect in other tissues hinges on the relative sensitivity of the erythropoietic system
compared with other systems. For example, one study of rats exposed to low levels of lead
over their lifetime demonstrated that protoporphyrin accumulation in renal tissue was already
significant at levels of lead exposure where little change was seen in erythrocyte porphyrin
levels. The issue of sensitivity is obviously distinct from the question of which system is
most accessible to measurement of the effect.
Other steps in the heme biosynthesis pathway are also known to be affected by lead, al-
though these have not been studied as much on a biochemical or molecular level. Levels of
coproporphyrin are increased in urine, reflecting active lead intoxication. Lead also affects
the activity of the enzyme uroporphyrinogen-I-synthetase, resulting in an accumulation of its
substrate, porphobilinogen. It has been reported that the erythrocyte enzyme is much more
sensitive to lead than the hepatic species and presumably accounts for much of the accumulated
substrate.
Anemia is a manifestation of chronic lead intoxication, being characterized as mildly
hypochromic and usually normocytic. It is associated with reticulocytosis, owing to shortened
cell survival, and the variable presence of basophilic stippling. Its occurrence is due to
both decreased production and increased rate of destruction of erythrocytes. In children
under four years of age, the anemia of Iron deficiency is exacerbated by the effect of lead,
and vice versa. Hemoglobin production is negatively correlated with blood lead in young chil-
dren, where iron deficiency may be a confounding factor, as well as in lead workers. In one
study, blood lead values that were usually below 80 ng/dl were inversely correlated with hemo-
globin content. In these subjects, iron deficiency was found to be absent. The blood lead
threshold for reduced hemoglobin content is about 50 Mfl/dl in adult lead workers and somewhat
lower In children, around 40 pg/dl.
The mechanism of lead-associated anemia appears to be a combination of reduced hemoglobin
production and shortened erythrocyte survival because of direct cell Injury. Effects of lead
on hemoglobin production involve disturbances of both heme and globin biosynthesis. The hemo-
lytic component to lead-induced anemia appears to be due to increased cell fragility and in-
creased osmotic resistance. In one study using rats, it was noted that the reduced cell
deformability and consequent hemolysis associated with vitamin E deficiency 1s exacerbated by
lead exposure. The molecular basis for increased cell destruction rests with inhibition of
(Na+, K+)~ATPase and pyrim1dine-5'-nucleotidase. Inhibition of the former enzyme leads to
cell "shrinkage," and inhibition of the latter results in impaired pyrimldlne nucleotide
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phosphorolysis and disturbance of the activity of the purine nucleotides necessary for
cellular energetics.
Tetraethyl lead and tetraroethyl lead, components of leaded gasoline, undergo transforma-
tion |n vivo to the neurotoxic trialkyl metabolites as well as further conversion to inorganic
lead. Hence, one might anticipate that exposure to such agents may show effects commonly
associated with inorganic lead in terms of heme synthesis and erythropoiesls.
Various surveys and case reports make It clear that the habit of sniffing leaded gasoline
is associated with chronic lead intoxication in children from socially deprived backgrounds in
rural or remote areas. Notable in these subjects is evidence of impaired heme biosynthesis as
indexed by significantly reduced ALA-D activity. In a number of case reports of frank lead
toxicity fran habitual sniffing of leaded gasoline, such effects as basophilic stippling in
erythrocytes and significantly reduced hemoglobin have also been noted.
Lead-associated disturbances of heme biosynthesis as a possible factor 1n the neuro-
logical effects of lead have been the object of considerable interest because of (1) the
recognized similarity between the classical signs of lead neurotoxicity and a number of the
neurological components of the congenital disorder known as acute intermittent porphyria, as
well as (2) some of the unusual aspects of lead neurotoxicity. There are two possible points
of connection between lead's effects on both heme biosynthesis and the nervous system. Con-
cerning the similarity of lead neurotoxicity to acute intermittent porphyria, there is the
common feature of excessive systemic accumulation and excretion of ALA. Second, lead neuro-
toxicity reflects, to some degree, impaired synthesis of heme and hemoproteins involved in
crucial cellular functions. Available information Indicates that ALA levels are elevated in
the brain of lead-exposed animals, arising via in situ inhibition of brain ALA-D activity or
via transport to the brain after formation in other tissues. ALA is known to traverse the
blood-brain barrier. Hence, ALA is accessible to, or formed within, the brain during lead ex-
posure and may express its neurotoxic potential.
Based on various In vitro and in vivo data obtained in the context of neurochemical
studies of lead neurotoxicity, it appears that ALA can readily play a role in GABAergic func-
tion, particularly inhibiting release of the neurotransmitter GABA from presynaptic receptors,
where ALA appears to be very potent even at low levels. In an in vitro stucfy, agonist
behavior by ALA was demonstrated at levels as low as 1.0 pM ALA. This in vitro observation
supports results of a study using lead-exposed rats in which there was reported inhibition of
both resting and K+-stimulated preloaded 3H-GABA. Further evidence for an effect of some
agent other than lead acting directly is the observation that in vivo effects of lead on
neurotransmitter function cannot be duplicated with in vitro preparations to which lead is
added. Human data on lead-Induced associations between disturbed heme synthesis and neuro-
toxicity, while limited, also suggest that ALA may function as a neurotoxicant.
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The connection of impaired heme and hemoproteln synthesis in the brain of the neonatal
rat was noted earlier. In these studies there was reduced cytochrome C production and im-
paired operation of the cytochrome C respiratory chain. Hence, one might expect that such
impairment would be most prominent in areas of relatively greater cellularization, such as the
hippocampus. As noted in Chapter 10, these are also regions where selective lead accumulation
appears to occur.
1.12.4 Neurotoxic Effects of Lead
An assessment of the impact of lead on human and animal neurobehavioral function raises
a number of issues. Among the key points addressed here are: (1) the internal exposure
levels, as indexed by blood lead levels, at which various adverse neurobehavioral effects
occur; (2) the reversibility of such deleterious effects; and (3) the populations that appear
to be most susceptible to neural damage. In addition, the question arises as to the utility
of using animal studies to draw parallels to the human condition.
1.12.4.1 Internal Lead Levels at which Neurotoxic Effects Occur. Markedly elevated blood
lead levels are associated with the most serious neurotoxic effects of lead exposure
(including severe, Irreversible brain damage as indexed by the occurrence of acute or chronic
encephalopathic symptoms, or both) in both humans and animals. For most human adults, such
damage typically does not occur until blood lead levels exceed 120 ng/dl. Evidence does
exist, however, for acute encephalopathy and death occurring in some human adults at blood
lead levels of 100-120 jjg/dl- In children, the effective blood lead level for producing
encephalopathy or death is lower, starting at approximately 80-100 pg/dl. It should be
emphasized that, once encephalopathy occurs, death is not an improbable outcome, regardless of
the quality of medical treatment available at the time of acute crisis. In fact, certain
diagnostic or treatment procedures themselves may exacerbate matters and push the outcome
toward fatality if the nature and severity of the problem are not diagnosed or fully recog-
nized. It is also crucial to note the rapidity with which acute encephalopathic symptoms can
develop or death can occur in apparently asymptomatic individuals or in those apparently only
mildly affected by elevated lead body burdens. Rapid deterioration often occurs, with
convulsions or coma suddenly appearing with progression to death within 48 hours. This
strongly suggests that even in apparently asymptomatic individuals, rather severe neural
damage probably exists at high blood lead levels even though it is not yet overtly manifested
in obvious encephalopathic symptoms. This conclusion is further supported by numerous studies
showing that overtly lead intoxicated children with high blood lead levels, but not observed
to manifest acute encephalopathic symptoms, are permanently cognitlvely Impaired, as are most
children who survive acute episodes of frank lead encephalopathy.
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Recent studies show that overt signs and symptoms of neurotoxicity (indicative of both
CNS and peripheral nerve dysfunction) are detectable in some human adults at blood lead levels
as low as 40-60 levels well below the 60 or 80 |jg/d1 criteria previously discussed as
being "safe" for adult lead exposures. In addition, certain electrophysiological studies of
peripheral nerve function in lead workers, indicate that slowing of nerve conduction veloc-
ities in some peripheral nerves are associated with blood lead levels as low as 30-50 pg/dl
(with no clear threshold for the effect being evident). These results are indicative of
neurological dysfunctions occurring at relatively low lead levels in non-overtly lead intoxi-
cated adults.
Other evidence tends to confirm that neural dysfunctions exist in apparently asymptomatic
children, at similar or even lower levels of blood lead. The body of studies on low-or
moderate-level lead effects on neurobehavioral functions in non-overtly lead intoxicated child-
ren, as evaluated in Chapter 12, presents an array of data pointing to that conclusion.
Several wel1-control 1ed studies have found effects that are clearly statistically significant,
whereas other have found nonsignificant but borderline effects. Some studies reporting gener-
ally nonsignificant findings at tiroes contain data confirming some statistically significant
effects, which the authors attribute to various extraneous factors. It should also be noted
that, given the apparent nonspecific nature of some of the behavioral or neural effects proba-
ble at low levels of lead exposure, one would not expect to find striking differences in every
instance. The lowest observed blood lead levels associated with significant neurobehavioral
deficits indicative of CNS dysfunction, both in apparently asymptomatic children and in devel-
oping rats and monkeys generally appear to be in the range of 30-50 yg/dl. However, other
types of neurotoxic effects, e.g., altered EEG patterns, have been reported at lower levels,
supporting a continuous dose-response relationship between lead and neurotoxicity. Such ef-
fects, when combined with adverse social factors (such as low parental IQ, low socioeconomic
status, poor nutrition, and poor quality of the caregiving environment) can place children,
especially those below the age of three years, at significant risk. However, it must be
acknowledged that nutritional covariates, as well as demographic social factors, have been
poorly controlled in many of the human studies reviewed. Socioeconomic status also is a crude
measure of parenting and family structure that requires further assessment as a possible con-
tributor to observed results of neurobehavioral studies.
Timing, type, and duration of exposure are important factors in both animal and human
studies. It is often uncertain whether observed blood lead levels represent the levels that
were responsible for observed behavioral deficits or electrophysiological changes. Monitoring
of lead exposures in human subjects in all cases has been highly intermittent or nonexistent
during the period of life preceding neurobehavioral assessment. In most human studies, only
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one or two blood lead values are provided per subject. Tooth lead nay be an Important cumula-
tive exposure Index, but its modest, highly variable correlation to blood lead or FEP and to
external exposure levels makes findings from various studies difficult to compare quantita-
tively. The complexity of the many important covariates and their interaction with dependent
variable measures of modest validity, e.g., IQ tests, may also account for some discrepancies
among the different studies.
1.12.4.2 Early Development and the Susceptibility to Neural Damage. On the question of early
childhood vulnerability, the neurobehavioral data are consistent with morphological and bio-
chemical studies of the susceptibility of the heme biosynthetlc pathway to perturbation by
lead. Various lines of evidence suggest that the order of susceptibility to lead's effects
is: (1) young > adults and (2) female > male. Animal studies also have pointed to the peri-
natal period of ontogeny as a particularly critical time for a variety of reasons; (1) it is
a period of rapid development of the nervous system; (2) It is a period where good nutrition
is particularly critical; and (3) it is a period where the caregiver environment is vital to
normal development. However, the precise boundaries of a critical period are not yet clear
and may vary depending on the species and function or endpoint that is being assessed. Never-
theless, there is general agreement that human Infants and toddlers below the age of three
years are at special risk because of in utero exposure, increased opportunity for exposure
because of normal mouthing behavior, and increased rates of lead absorption due to various
factors, e.g., nutritional deficiences.
1.12.4.3 The Question of Irreversibility. Little research on humans is available on persis-
tence of effects. Some work suggests that mild forms of peripheral neuropathy 1n lead workers
may be reversible after termination of lead exposure, but little is known regarding the rever-
sibility of lead effects on central nervous system function in humans. A recent two-year
follow-up study of 28 children of battery factory workers found a continuing relationship
between blood lead levels and altered slow wave voltage of cortical slow wave potentials indic-
ative of persisting CNS effects of lead. Current population studies, however, will have to be
supplemented by prospective longitudinal studies of the effects of lead on development in
order to address the issue of reversibility or persistence of lead neurotoxic effects in
humans more satisfactorily.
Various animal studies provide evidence that alterations in neurobehavioral function may
be long-lived, with such alterations being evident long after blood lead levels have returned
to control levels. These persistent effects have been demonstrated in monkeys as well as rats
under a variety of learning performance test paradigms. Such results are also consistent with
morphological, electrophysiological, and biochemical studies on animals that suggest lasting
changes in synaptogenesis, dendritic development, myelin and fiber tract formation, ionic
mechanisms of neurotransmission, and energy metabolism.
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1.12.4.4 Utility of Animal Studies In Drawing Parallels to the Hunan Condition. Animal
models are used to shed light on questions where it is Impractical or ethically unacceptable
to use human subjects. This is particularly true in the case of exposure to environmental
toxins such as lead. In the case of lead, it has been effective and convenient to expose
developing animals via their mothers' milk or by gastric gavage, at least until weaning. In
many studies, exposure was continued in the water or food for some time beyond weaning. This
approach simulates at least two features commonly found in human exposure: oral intake and
exposure during early development. The preweaning period in rats and mice is of particular
relevance to in terms of parallels with the first two years or so of human brain development.
However, important questions exist concerning the comparability of animal models to
humans. Given differences between humans, rats, and monkeys in heme chemistry, metabolism,
and other aspects of physiology and anatomy, it is difficult to state what constitutes an
equivalent internal exposure level (much less an equivalent external exposure level). For
example, is a blood lead level of 30 pg/dl in a suckling rat equivalent to 30 pg/dl in a
three-year-old child? Until an answer is available to this question, I.e., until the function
describing the relationship of exposure indices in different species is available, the utility
of animal models for deriving dose-response functions relevant to humans will be limited.
Questions also exist regarding the comparability of neurobehavioral effects in animals
with human behavior and cognitive function. One difficulty in comparing behavioral endpolnts
such as locomotor activity is the lack of a consistent operational definition. In addition to
the lack of standardized methodologies, behavior is notoriously difficult to "equate" or com-
pare meaningfully across species because behavioral analogies do not demonstrate behavioral
homologies. Thus, it is improper to assume, without knowing more about the responsible under-
lying neurological structures and processes, that a rat's performance on an operant condition-
ing schedule or a monkey's performance on a stimulus discrimination task corresponds to a
child's performance on a cognitive function test. Still deficits in performance on such tasks
are Indicative of altered CNS function which 1s likely to parallel some type of altered human
CNS function as well.
In terms of morphological findings, there are reports of hippocampal lesions in both
lead-exposed rats and humans that are consistent with a number of behavioral findings suggest-
ing an impaired ability to respond appropriately to altered contingencies for rewards. That
is, subjects tend to persist 1n certain patterns of behavior even when changed conditions make
the behavior inappropriate. Other morphological findings in animals, such as demyelination
and glial cell decline, are comparable to human neuropathology observations mainly at rela-
tively high exposure levels.
Another neurobehavioral endpoint of Interest 1n comparing human and animal neurotoxicity
of lead is electrophysiological function. Alterations of electroencephalographic patterns and
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cortical slow wave voltage have been reported for lead-exposed children, and various electro-
physiological alterations both In vivo (e.g., in rat visual evoked response) and in vitro
(e.g., in frog miniature endplate potentials) have also been noted in laboratory animals. At
this time, however, these lines of work have not converged sufficiently to allow for strong
conclusions regarding the electrophysiological aspects of lead neurotoxicity.
Biochemical approaches to the experimental study of leads effects on the nervous system
have generally been limited to laboratory animal subjects. Although their linkage to human
neurobehavioral function is at this point somewhat speculative, such studies do provide in-
sight to possible neurochemical intermediaries of lead neurotoxicity. No single neurotrans-
mitter system has been shown to be particularly sensitive to the effects of lead exposure;
rather, lead-induced alterations have been demonstrated in several different neurotransmitter
systems, including dopamine, norepinephrine, serotonin, and gamma-aminobutyric acid. In addi-
tion, lead has been shown to have subcellular effects 1n the central nervous system at the
level of mitochondrial function and protein synthesis.
Given the above-noted difficulties in formulating a comparative basis for internal expo-
sure levels among different species, the primary value of many animal studies, particularly In
vitro studies, may be in the information they can provide on basic mechanisms involved in lead
neurotoxicity. A number of In vitro studies show that significant, potentially deleterious
effects on nervous system function occur at In situ lead concentrations of 5 pM and possibly
lower, suggesting that no threshold may exist for certain neurochemical effects of lead on a
subcellular or molecular level. The relationship between blood lead levels and lead concen-
trations at such extra- or Intracellular sites of action, however, remains to be determined.
Despite the problems 1n generalizing from animals to humans, both the animal and the human
studies show great internal consistency 1n that they support a continuous dose-response
functional relationship between lead and neurotoxic biochemical, morphological, electrophysio-
logical, and behavioral effects.
1.12.5 Effects of Lead on the Kidney
It has been known for more than a century that kidney disease can result from lead
poisoning. Identifying the contributing causes and mechanisms of lead-induced nephropathy has
been difficult, however, in part because of the complexities of human exposure to lead and
other nephrotoxic agents.
Nevertheless, it is possible to estimate at least roughly lead exposure ranges associated
with detectable renal dysfunction 1n both human adults and children. More specifically,
numerous studies of occupationally exposed workers have provided evidence for lead-Induced
chronic nephropathy being associated with blood lead levels ranging from 40 to more than
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100 M9/dl• and some are suggestive of renal effects possibly occurring even at levels as low
as 30 pg/dl. Similarly, in children, the relatively sparse evidence available points to the
manifestation of renal dysfunction, as indexed for example by generalized aminoaciduria, at
blood lead levels across the range of 40 to more than 100 pg/dl. The current lack of evidence
for renal dysfunction at lower blood lead levels in children may simply reflect the greater
clinical concern with neurotoxic effects of lead intoxication in children. The persistence of
lead-induced renal dysfunction in children also remains to be more fully investigated, al-
though a few studies Indicate that children diagnosed as being acutely lead poisoned experi-
ence lead nephropathy effects lasting throughout adulthood.
Parallel results from experimental animal studies reinforce the findings 1n humans and
help illuminate the mechanisms underlying such effects. For example, a number of transient
effects 1n human and animal renal function are consistent with experimental findings of revers-
ible lesions such as nuclear Inclusion bodies, cytomegaly, swollen mitochondria, and increased
numbers of iron-containing lysosomes in proximal tubule cells. Irreversible lesions such as
interstitial fibrosis are also well documented 1n both humans and animals following chronic
exposure to high doses of lead. Functional renal changes observed in humans have also been
confirmed in animal model systems with respect to increased excretion of amino acids and
elevated serum urea nitrogen and uric acid concentrations. The inhibitory effects of lead
exposure on renal blood flow and glomerular filtration rate are currently less clear 1n exper-
imental model systems; further research is needed to clarify the effects of lead on these
functional parameters 1n animals. Similarly, while lead-induced perturbation of the renin-
angiotensin system has been demonstrated in experimental animal models, further research 1s
needed to clarify the exact relationships among lead exposure (particularly chronic low-level
exposure), alteration of the renin-angiotensin system, and hypertension in both humans and
animals.
On the biochemical level, it appears that lead exposure produces changes at a number of
sites. Inhibition of membrane marker enzymes, decreased mitochondrial respiratory function/
cellular energy production, Inhibition of renal heme biosynthesis, and altered nucleic acid
synthesis are the most marked changes to have been reported. The extent to which these mito-
chondrial alterations occur 1s probably mediated in part by the intracellular bioavailability
of lead, which is determined by its binding to high affinity kidney cytosolic binding proteins
and deposition within intranuclear inclusion bodies.
Recent studies in humans have indicated that the EDTA lead-mobilization test is the most
reliable technique for detecting persons at risk for chronic nephropathy. Blood lead measure-
ments are a less satisfactory indicator because they may not accurately reflect cumulative
absorption some time after exposure to lead has terminated.
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A number of major questions remain to be more definitively answered concerning the effect
of lead on the kidney. Can a distinctive lead-induced renal lesion be identified either in
functional or histologic terms? What biologic measurements are most reliable for the predic-
tion of lead-induced nephropathy? What is the incidence of lead nephropathy in the general
population as well as among specifically defined subgroups with varying exposure? What 1s the
natural history of treated and untreated lead nephropathy? What is the mechanism of lead-
induced hypertension and renal Injury? What are the contributions of environmental and
genetic factors to the appearance of renal injury due to lead? At what level of lead in blood
can the kidneys be affected? Is there a threshold for renal effects of lead? The most dif-
ficult question to answer nay well be to determine the contribution of low levels of lead
exposure to renal disease of non-lead etiologies.
1-12.6 Effects of Lead on Reproduction and Development
Data from human and animal studies Indicate that lead nay exert gametotoxic, embryotoxic,
and (according to some animal studies) teratogenic effects that nay influence the survival and
development of the fetus and newborn. Prenatal viability and development, it appears, nay
also be affected indirectly, contributing to concern for unborn children and, therefore, preg-
nant women or childbearing-age women being groups at special risk for lead effects. Early
studies of quite high dose lead exposure in pregnant women Indicate toxic—but not tera-
togenic—effects on the conceptus. Effects on reproductive performance in women at lower
exposure levels are not well documented. Unfortunately, currently available human data
regarding lead effects on the fetus during development generally do not lend themselves to
accurate estimation of lowest observed or no-effect levels. However, some studies have shown
that fetal heme synthesis 1s affected at maternal and fetal blood lead levels as low as
approximately 15 jjfl/dl, as Indicated by urinary ALA levels and ALA-D activity. This observed
effect level 1s consistent with lowest observed effect levels for indications of altered heme
synthesis seen at later ages for preschool and older children.
There are currently no reliable data pointing to adverse effects in human offspring fol-
lowing paternal exposure to lead, but' industrial exposure of men to lead at levels resulting
in blood lead values of 40-50 pg/dl appear to have resulted in altered testicular function.
Also, another study provided evidence of effects on prostatic and seminal vesicle functions at
40-50 ng/dl blood lead levels in lead workers.
The paucity of human exposure data force an examination of the animal studies for Indica-
tions of threshold levels for effects of lead .on the conceptus. It must be noted that the
animal data are almost entirely derived from rodents. Based on these rodent data, it seems
likely that fetotoxic effects have occurred in animals at chronic exposures to 600-1000 ppn
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lead in the diet. Subtle effects on fetal physiology and metabolism appear to have been ob-
served in rats after chronic maternal exposure to 10 ppm lead in drinking water, while similar
effects of inhaled lead have been seen at chronic levels of 10 pg/m3. With acute exposure by
gavage or by injection, the values are 10-16 mg/kg and 16-30 mg/kg, respectively. Since
humans are most likely to be exposed to lead in their diet, air, or water, the data from other
routes of exposure are of less value in estimating harmful exposures. Indeed, it seems likely
that teratogenic effects occur only when the maternal dose is given by injection.
Although human and animal responses may be dissimilar, the animal evidence does document
a variety of effects of lead exposure on reproduction and development. Measured or apparent
changes in production of or response to reproductive hormones, toxic effects on the gonads,
and toxic or teratogenic effects on the conceptus have all been reported. The animal data
also suggest subtle effects on such parameters as metabolism and cell structure that should be
monitored 1n human populations. Well designed human epidemiological studies involving large
numbers of subjects are still needed. Such data could clarify the relationship of exposure
levels and durations to blood lead values associated with significant effects, and are needed
for estimation of no-effect levels.
Given that the most clear-cut data concerning the effects of lead on reproduction and
development are derived from studies employing high lead doses in laboratory animals, there is
still a need for more critical research to evaluate the possible subtle toxic effects of lead
on the fetus, using biochemical, ultrastructural, or neurobehavioral endpoints. An exhaustive
evaluation of lead-associated changes in offspring will require consideration of possible
additional effects due to paternal lead burden. Neonatal lead intake via consumption of milk
from lead-exposed mothers may also be a factor at times. Also, it must be recognized that
lead effects on reproduction may be exacerbated by other environmental factors (e.g., dietary
influences, maternal hyperthermia, hypoxia, and co-exposure to other toxins).
1.12.7. Genotoxic and Carcinogenic Effects of lead
It 1s difficult to conclude what role lead may play 1n the induction of human neoplasia.
Epidemiological studies of lead-txposed workers provide no definitive findings. However, sta-
tistically significant elevations in cancer of the respiratory tract and digestive system in
workers exposed to lead and other agents warrant some concern. Since it Is clear that lead
acetate can produce renal tumors in some experimental animals, 1t seems reasonable to conclude
that at least that particular lead compound should be regarded as a carcinogen and prudent to
treat it as if it were also human carcinogen (as per IARC conclusions and recommendations).
However, this statement is qualified by noting that lead has been seen to Increase tumorogen-
esis rates in animals only at relatively high concentrations, and therefore does not seem to
be an extremely potent carcinogen. In vitro studies further support the genotoxic and carcin-
ogenic role of lead, but also indicate that lead is not extremely potent in these systems.
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1-12.8. Effects of Lead on the I—une System
Lead renders animals highly susceptible to endotoxins and infectious agents. Host sus-
ceptibility and the humoral Immune system appear to be particularly sensitive. As postulated
1n recent studies, the macrophage may be the primary immune target cell of lead. Lead-induced
immunosuppression occurs at low lead exposures (blood lead levels in the 20-40 pg/dl range)
that, although they induce no overt toxicity, may nevertheless be detrimental to health.
Available data provide good evidence that lead affects Immunity, but additional studies are
necessary to elucidate the actual mechanisms by which lead exerts its Immunosuppressive action.
Knowledge of lead effects on the human immune system is lacking and must be ascertained in
order to determine permissible levels for human exposure. However, in view of the fact that
lead affects Immunity in laboratory animals and 1s immunosuppressive at very low dosages, Its
potential for serious effects 1n humans should be carefully considered.
1.12.9 Effects of Lead on Other Organ Systems
The cardiovascular, hepatic, endocrine, and gastrolntestional systems generally show
signs of dysfunction mainly at relatively high lead exposure levels. Consequently, 1n most
clinical and experimental studies attention has been primarily focused on more sensitive and
vulnerable target organs, such as the hematopoietic and nervous systems. However, it should
be noted that overt gastrointestinal symptoms associated with lead Intoxication have been
observed' in some recent studies to occur in lead workers at blood lead levels as low as 40-
60 |jg/ suggesting that effects on the gastrointestinal and the other above organ systems
may occur at relatively low exposure levels but remain to be demonstrated by future scientific
investigations.
1.13 EVALUATION OF HUMAN HEALTH RISKS ASSOCIATED WITH EXPOSURE TO LEAD AND ITS COMPOUNDS
1.13.1 Introduction
This section attempts to integrate, concisely, key information and conclusions discussed
1n preceding sections into a coherent framework by which interpretation and judgments can be
made concerning the risk to human health posed by present levels of lead contamination in the
United States.
In regard to various health effects of lead, the main emphasis here is on the identifica-
tion of those effects most relevant to various segments of the general U.S. population and the
placement of such effects in a dose-effect/dose-response framework. In regard to the latter,
a crucial issue has to do with relative response of various segments of the population 1n
terms of effect thresholds as indexed by some exposure Indicator. Furthermore, it is of
Interest to assess the extent to which available information supports the notion of a conti-
nuum of effects as one proceeds across the spectrum of exposure levels. Finally, it is of
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interest to ascertain the availability of data on the relative number or percentage of members
(i.e., "responders") of specific population groups that can be expected to experience a par-
ticular effect at various lead exposure levels in order to permit delineation of dose-response
curves for the relevant effects in different segments of the population. These matters are
discussed in Sections 1.13,5 and 1.13.6.
Melding of information from the sections on lead exposure, metabolism, and biological
effects permits the identification of population segments at special risk in terms of physio-
logical and other host characteristics, as well as heightened vulnerability to a given effect;
and these risk groups are discussed in Section 1.13.7, With demographic identification of
Individuals at risk, one may then draw upon population data from other sources to obtain a
numerical picture of the magnitude of population groups at potential risk. This is also dis-
cussed in Section 1.13.7.
1.13.2 EXPOSURE ASPECTS
1.13.2.1 Levels of Lead in Various Media of Relevance to Human Exposure
Human populations in the United States are exposed to lead in air, food, water, and dust.
In rural areas, Americans not occupationally exposed to lead consume SO to 75 jjg Pb/day. This
level of exposure is referred to as the baseline exposure because it is unavoidable except by
drastic change in lifestyle or by regulation of lead in foods or ambient air. There are
several environmental circumstances that can increase human exposures above baseline levels.
Most of these circumstances involve the accumulation of atmospheric dusts in the work and play
environments. A few, such as pica and family home gardening, may involve consumption of lead
from chips of exterior or interior house paint.
Ambient Air Lead Levels. Monitored ambient air lead concentration values in the U.S. are
contained in two principal data bases: (1) EPA's National A1r Sampling Network (NASN),
recently renamed National Filter Analysis Network (NFAN); and (2) EPA's National Aerometric
Data Bank, consistting of measurements by state and local agencies in conjunction with compli-
ance mpnitoring for the current ambient air lead standard.
NASN data for 1982, the most current year in the annual surveys, indicate that most of
the urban sites show reported annual averages below 0.7 jig Pb/m3, while the majority of the
non-urban locations have annual figures below 0.2 h9 Pb/m3. Over the interval 1976-1981,
there has been a downward trend in these averages, mainly attributable to decreasing lead
content of leaded gasoline and the increasing usage of lead-free gasoline. Furthermore,
examination of quarterly averages over this interval shows a typical seasonal variation,
characterized by maximum air lead values in winter and minimum values in summer.
With respect to the particle size distribution of ambient air lead, EPA studies using
cascade impactors in six U.S. cities have indicated that 60 to 75 percent of such air lead was
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associated with sub-micron particles. This size distribution is significant In considering
the distance particles may be transported and the deposition of particles in the pulmonary
compartment of the respiratory tract. The relationship between airborne lead at the monitor-
ing station and the lead inhaled by humans is complicated by such variables as vertical
gradients, relative positions of the source, monitor, and the person, and the ratio of indoor
to outdoor lead concentrations- To obtain an accurate picture of the amount of lead inhaled
during the normal activities of an individual, personal monitors would probably be the most
effective. But the information gained would be insignificant, considering that inhaled lead
is only a small fraction of the total lead exposure, compared to the lead In food, beverages,
and dust. The critical question with respect to airborne lead is how much lead becomes
entrained in dust. In this respect, the existing monitoring network may provide an adequate
estimate of the air concentration from which the rate of deposition can be determined. The
percentage of ambient air lead which represents alkyl forms was noted in one study to range
from 0.3 to 2.7 percent, rising up to about 10 percent at service stations.
Levels of Lead In Dust. The lead content of dusts can figure prominently in the total
lead exposure picture for young children. Lead in aerosol particles deposited on rigid sur-
faces in urban areas (such as sidewalks, porches, steps, parking lots, etc.) does not undergo
dilution compared to lead transferred by deposition onto soils. Dust can approach extremely
high concentrations. Dust lead can accumulate in the interiors of dwellings as well as in the
outside surroundings, particularly in urban areas.
Measurements of soil lead to a depth of 5 cm in areas of the U.S., using sites near road-
ways, were shown in one study to range from 150 to 500 pg Pb/g dry weight close to roadways
(i.e., within 8 meters). By contrast, lead in dusts deposited on or near heavily traveled
traffic arteries show levels in major U.S. cities ranging up to 8000 MS Pb/g and higher. In
residential areas, exterior dust lead levels are 1000 pg/g or less. Levels of lead in house
dust can be significantly elevated. A study of house dust samples in Boston and New York City
revealed levels of 1000 to 2000 pg Pb/g. Some soils adjacent to houses with exterior lead-
based paints may have lead concentrations greater than 10,000
Thirty-four percent of the baseline consumption of lead by children comes from the con-
sumption of 0.1 g of dust per day (Tables 1-13 and 1-14). Ninety percent of this dust lead is
of atmospheric origin. Dust also accounts for more than ninety percent of the additive lead
attributable to residences in an urban environment or near a smelter (Table 1-15).
Levels of Lead 1n Food. The route by which adults and older children in the baseline
population of the U.S. receive the largest proportion of lead intake is through foods, with
reported estimates of the dietary lead intake for Americans ranging from 60 to 75 pg/day.
The added exposure from living in an urban environment is about 30 Mfl/d'y for adults and 100
pg/day for children, all of which can be attributed to atmospheric lead.
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TABLE 1-13. SUMMARY OF BASELINE HUMAN EXPOSURES TO LEADt
Soil
Source
Total
Lead
Consumed
Percent
of
Total
Consumption
Natural
Lead
Consumed
Indirect
Atmospheric
Lead*
Direct
Atmospheric
Lead*
Lead froa
Solder or
Other Metals
Lead of
Undetermined
Origin
Child 2-yr old
Inhaled Air 0.5
Food 28.7
Water & beverages 11.2
Oust 21.0
Total 61.4
Percent 100%
Adult female
Inhaled Air
Food
Water & beverages
Oust
Total 56.6
Percent 100*
Adult male
Inahaled air 1.0
Food 45.7
Water & beverages 25.1
Dust _4i5
Total 76.3
Percent 100*
0.8%
46.7
18.3
34.2
1.8%
58.7
31.6
7.9
0.001
0.9
0.01
0.6
1.5
2.4%
0.002
1.0
0.01
0.2
1.2
2. IX
0.002
1.4
0.1
0.2
1.7
2.2%
0.9
2.1
3.0
4.9%
1.0
3.4
4.4
7.8%
1.4
4.7
6.1
8.0%
31.6
51.5%
1.0
17.4
2.8
2.9
24.1
31.6%
10.3
7.8
18.1
29.5%
11.9
12.5
24.4
43.1%
16.4
17.5
33.9
44.4%
17.6
1.4
19.0
22.6%
21.6
1.4
23.0
26.8%
31.5
1.4
32.9
27.1%
"Indirect atmospheric lead has been previously incorporated into soil, and will probably regain in the soil for decades or
longer. Direct atmospheric lead has been deposited on the surfaces of vegetation and living areas or incorporated during
food processing shortly before human consumption. It may be assumed that 85 percent of direct atmospheric lead derives
from gasoline additives.
tun its are in pg/d«y.
-------
PRELIMINARY DRAFT
TABLE 1-14. RELATIVE BASELINE HUMAN LEAD EXPOSURES EXPRESSED PER KILOGRAM BODY WEIGHT*
Total
Lead
Consumed
Total Lead Consumed
Per Kg Body Wt
jig/Kg-Day
Atmospheric Lead
Per Kg Body wt
jjg/Kg • Day
Child (2 yr old)
(pg/day)
/
Inhaled air
0.5
0.05
0.05
Food
28.7
2.9
1.1
Water and beverages
11.2
1.1
0.12
Dust
21.0
2.1
1.9
Total
61.4
6.15
3.17
Adult female
Inhaled air
1.0
0.02
0.02
Food
33.2
0.66
0.25
Water and beverages
17.9
0.34
0,04
Dust
4.5
0.09
0.06
Total
56.6
1.13
0.37
Adult male
Inhaled air
1.0
0.014
0.014
Food
45.7
0.65
0.25
Water and beverages
25.1
0.36
0.04
Dust
4.5
0.064
0.04
Total
76.3
1.088
0.344
*Boc(y weights: 2 year old child = 10/kg; adult female » 50 kg; adult male = 70 kg.
Atmospheric lead may be added to food crops In the field or pasture, during transporta-
tion to the market, during processing, and during kitchen preparation. Metallic lead, mainly
solder, may be added during processing and packaging. Other sources of lead, as yet undeter-
mined, increase the lead content of food between the field and dinner table. American
children, adult females, and adult males consume 29, 33 and 46 |jg Pb/day, respectively, in
milk and nonbeverage foods. Of these amounts, 38 percent is of direct atmospheric origin, 36
percent is of metallic origin and 20 percent 1s of undetermined origin.
Processing of foods, particularly canning, can significantly add to their background lead
content, although it appears that the impact of this is being lessened with the trend awfiy
from use of lead-soldered cans. The canning process can increase lead levels 8-to 10-fold
higher than for the corresponding uncanned food items. Home food preparation can also be a
source of additional lead in cases where food preparation surfaces are exposed to moderate
amounts of high-lead household dust.
CHPD1/A 1-127 9/30/83
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TABLE 1-15. SUMMARY OF POTENTIAL ADDITIVE EXK9SU8ES TO LEAD
Total
Ataospherlc
Other
Lead
Lead
Lead
Consuaed
Corwuaed
Sources
(jig/day)
(MO/day)
(tig/day)
¦asellne exposure:
CM Id (2 yr old)
Inhaled air
0.5
0.5
-
Food, inter & beverages
39.9
12.1
27.8
Oust
21.0
18.0
2.0
Total baseline
61.4
31.6
29.8
Additional exposure due to:
urban ataospheres;1
air Inhalation
7
7
0
dust
72
71
1
faally gardens*
800
200
600
Interior lead paint1
85
-
85
residence near saelter:4
air Inhalation
60
60
-
dust
2250
2250
-
secondary occupational*
150
-
8asel1ne exposure:
Adult Male
Inhaled air
1.0
1.0
-
food, water & beverages
70.8
20.2
so.*
Dust
4.5
2.9
1,6
Total baseline
78.3
24.1
§2.2
Additional exposure due to;
urfean ataospheres:1
air Inhalation
14
14
-
dust
7
7
-
faally gardens2
2000
500
1500
Interior lead paint*
17
-
17
residence near saelter:4
air Inhalation
120
120
-
dust
250
250
•
occupational*
1100
1100
-
secondary occifiatlonal*
21
-
•
smiting
30
27
3
Mine consumption
100
1
?
'Includes lead fro* household ind street dust (1000 mQ/9) «nd Inhaled air (.75 yg/ft*)
*assuaes tall lead concentration of MOO yg/g; *11 fresh leafy and root vegetables, sweat
corn of Table 7-15 replaced by produce froa garden. Also assuaes 25X of soil lead 1s of
ataospherlc origin.
'assiaes household dust rises froet 300 to 2000 (*g/g. Dust consumption reaalns the saae as
baseline. Does not Include conswptlon of paint chips.
4assuaes household and street dust Increases to 25,000 yg/g, Inhaled air increases to 6
4HJ/a*.
*assuae* household dust Increases to 2400 ug/0-
*astuaes 8 hr shift at 10 jms K>/a* or 90S efficiency of respirators at 100 (ig/ Pb/a*. and
occupational dusts at 100,000 pg/M*.
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Lead Levels in Drinking Water. Lead in drinking water may result from contamination of
the water source or from the use of lead materials in the water distribution system. Lead
entry into drinking water from the latter is increased in water supplies which are plumbo-
solvent, i.e., with a pH below 6.5. Exposure of individuals occurs through direct ingestion
of the water or via food preparation in such water.
The interim EPA drinking water standard for lead is 0.05 Hfl/fl (50 yg/1) and several
extensive surveys of public water supplies indicate that only a limited number of samples ex-
ceeded this standard on a nationwide basis. For example, a survey of interstate carrier water
supplies conducted by EPA showed that only 0.3 percent exceeded the standard.
The major source of lead contamination of drinking water is the distribution system it-
self, particularly in older urban areas. Highest levels are encountered in "first-draw" sam-
ples, I.e., water sitting in the piping system for an extended period of time. In a large
community water supply survey of 969 systems carried out in 1969-1970, it was found that the
prevalence of samples exceeding 0.01 pg/g was greater where water was plumbo-solvent.
Most drinking water, and the beverages produced from drinking water, contain 0.008 to
0.02 jjg Pb/g. The exceptions are canned juices and soda pop, which range from 0.033 to 0.052
Mg/g. About 11 percent of the lead consumed in drinking water and beverages is of direct
atmospheric origin, 70 percent comes from solder and other metals.
Lead in Other Media. Flaking lead paint in deteriorated housing stock in urban areas of
the Northeast and Midwest has long been recognized as a major source of lead exposure for
young children residing in this housing stock, particularly for children with pica. Indivi-
duals who are cigarette smokers may inhale significant amounts of lead in tobacco smoke. One
study has indicated that the smoking of 30 cigarettes daily results in lead intake equivalent
to that of inhaling lead in ambient air at a level of 1.0 |ig Pb/m3.
Cumulative Human Lead Intake From Various Sources. Table 1-13 shows the baseline of
human lead exposures as described in detail in Chapter 7. These data show that atmospheric
lead accounts for at least 30 percent of the baseline adult consumption and 50 percent of the
daily consumption by a 2 yr old child. These percentages are conservative estimates because a
part of the lead of undetermined origin may originate from atmospheric lead not yet accounted
for.
From Table 1-14, It can be seen that young children have a dietary lead intake rate, that
is 5-fold greater than for adults, on a body weight basis. To these observations must be
added that absorption rates for lead are higher in children than in adults by at least 3-fold.
Overall, then, the rate of lead entry into the blood stream of children, on a body weight
basis, is estimated to be twice that of adults from the respiratory tract and 6 and 9 times
greater from the GI tract. Since children consume more dust than adults, the atmospheric
fraction of the baseline exposure is ten-fold higher for children than for adults, on a body
CfiPDl/A 1-129 9/30/83
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weight basis. These differences generally tend to place young children at greater risk, in
terras of relative amounts of proportions of atmospheric lead absorbed per kg body weight, than
adults under any given lead exposure situation.
1.13.3 LEAD METABOLISM: KEY ISSUES FOR HUMAN HEALTH RISK EVALUATION
From the detailed discussion of those various quantifiable characteristics of lead toxi-
cokinetics in humans and animals presented in Chapter 10, several clear Issues emerge as being
important for full evaluation of the human health risk posed by lead:
(1) Differences in systemic or internal lead exposure of groups within the general popu-
lation in terms of such factors as age/development and nutritional status; and
(2) The relationship of indices of internal lead exposures to both environmental levels
of lead and tissues levels/effects.
Item 1 provides the basis for identifying segments within human populations at increased
risk in terms of exposure criteria and is used along with additional information on relative
sensitivity to lead health effects for identification of risk populations. The chief concern
with item 2 is the adequacy of current means for assessing internal lead exposure 1n terms of
providing adequate margins of protection from lead exposures producing health effects of con-
cern.
1.13.3.1 Differential Internal Lead Exposure Within Population Groups
Compared to adults, young children take in more lead through the gastrointestinal and
respiratory tracts on a unit body weight basis, absorb a greater fraction of this lead intake,
and also retain a greater proportion of the absorbed amount.
Unfortunately, such amplification of these basic toxicokinetic parameters in children vs.
adults also occurs at the time when: (1) humans are developmental 1y more vulnerable to the
effects of toxicants such as lead in terms of metabolic activity, and (2) the interactive re-
lationships of lead with such factors as nutritive elements are such as to induce a negative
course toward further exposure risk.
Typical of physiological differences in children vs. adults in terms of lead exposure im-
plications is a more raetabolically active skeletal system in children. In children, turnover
rates of bone elements such as calcium and phosphorus are greater than in adults, with corre-
spondingly greater mobility of bone-sequestered lead. This activity is a factor in the obser-
vation that the skeletal system of children is relatively less effective as a depository for
lead than in adults.
Metabolic demand for nutrients, particularly calcium, iron, phosphorus, and the trace
nutrients, is such that widespread deficiencies of these nutrients exist, particularly among
poor children. The interactive relationships of these elements with lead are such that defi-
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ciency states both enhance lead absorption/retention and, as in the case of lead-induced
reductions in l,25-d1hydroxyvita«iin D, establish increasingly adverse interactive cycles.
Quite apart from the physiological differences which enhance internal lead exposure in
children is the unique relationship of 2- to 3-year-olds to their exposure setting by way of
normal mouthing behavior and the extreme manifestation of this behavior, pica. This behavior
occurs in the same age group which studies have consistently identified as having a peak in
blood lead. A number of investigations have addressed the quantification of this particular
route of lead exposure, and 1t is by now clear that such exposure will dominate other routes
when the child's surroundings, e.g., dust and soil, are significantly contaminated by lead.
Information provided in Chapter 10 also makes it clear that lead traverses the human pla-
cental barrier, with lead uptake by the fetus occurring throughout gestation. Such uptake of
lead poses a potential threat to the fetus via an impact on the embryological developement of
the central nervous and other systems. Hence, the only logical means of protecting the fetus
from lead exposure is exposure control during pregnancy.
Within the general population, then, young children and pregnant women qualify as defin-
ale risk groups for lead exposure. Occupational exposure to lead, particularly among lead
workers, logically defines these individuals as being in a high-risk category; work place con-
tact 1s augmented by those same routes and levels of lead exposure affecting the rest of the
adult population. From a biological point of view, lead workers do not differ from the gene-
ral adult population with respect to the various toxicoklnetic parameters and any differences
in exposure control—occupational vs. non-occupational populations—as they exist are based on
factors other than toxicokinetics.
1.13.3.2 Indices of Internal Lead Exposure and Their Relationship To External Lead Levels and
Tissue Burdens/Effects
Several points are of importance in this area of lead toxicokinetics. They are: (1) the
temporal characteristics of indices of lead exposure; (2) the relationship of the indicators
to external lead levels; (3) the validity of Indicators of exposure 1n reflecting target tis-
sue burdens; (4) the interplay between these indicators and lead in body compartments; and
(5) those various aspects of the Issue with particular reference to children.
At this time, blood lead is widely held to be the most convenient, if imperfect, index of
both lead exposure and relative risk for various adverse health effects. In terms of ex-
posure, however, it is generally accepted that blood lead is a temporally variable measure
which yields an index of relatively recent exposure because of the rather rapid clearance of
absorbed lead from the blood. Such a measure, then, 1s of limited usefulness in cases where
exposure is variable or intermittent over time, as is often the case with pediatric lead ex-
posure.
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Mineralizing tissue, specifically deciduous teeth, accumulate lead over time in propor-
tion to the degree of lead exposure, and analysis of this material provides an assessment
integrated over a greater time period and of more value in detecting early childhood exposure.
These two methods of assessing internal lead exposure have obvious shortcomings. A blood
lead value will say little about any excessive lead intake at early periods, even though such
remote exposure may have resulted in significant injury. On the other hand, whole tooth or
dentine analysis is retrospective In nature and can only be done after the particularly vulne-
rable age in children under 4 to 5 years— has passed. Such a measure, then provides little
utility upon which to implement regulatory policy or clinical intervention.
The dilemmas posed by these existing methods may be able to be resolved by in situ analy-
sis of teeth and bone lead, such that the intrinsic advantage of mineral tissue as a cumula-
tive index is combined with measurement which is temporally concordant with on-going exposure.
Work in several laboratories offers promise for such in situ analysis (See Chapters 9 and 10).
A second issue concerning internal indices of exposure and environmental lead is the
relationship of changes in lead content of some medium with changes in blood content. Much of
Chapter 11 was given over to description of the mathematical relationships of blood lead with
lead in some external medium-- air, food, water, etc., without consideration of the biological
underpinnings for these relationships.
Over a relatively broad range of lead exposure through some medium, the relationship of
lead in the external medium to blood lead is curvilinear, such that relative change in blood
lead per unit change in medium level generally becomes increasingly less as exposure increases.
This behavior may reflect changes in tissue lead kinetics, reduced lead absorption, or in-
creased excretion. Limited animal data would suggest that changes in excretion or absorption
are not factors in this phenomenon. In any event, modest changes in blood levels with expo-
sure at the higher end of this range are in no way to be taken as reflecting concomitantly
modest changes in body or tissue lead uptake. Evidence continues to accumulate which suggests
that an indicator such as blood lead is an imperfect measure of tissue lead burdens and of
changes in such tissue levels in relation to changes in external exposure.
In Chapter 10, it was pointed out that blood lead is logarithmically related to chelata-
ble lead (the latter being a more useful measure of the potentially toxic fraction of body
lead), such that a unit change in blood lead is associated with an increasingly larger amount
of chelatable lead. One consequence of this relationship is that moderately elevated blood
lead values will tend to mask the "margin of safety" in terms of mobile body lead burdens.
Such masking is apparent in one study of children where chelatable lead levels in children
showing moderate elevations in blood lead overlapped those obtained in subjects showing frank
plumbism, i.e. overt lead intoxication.
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Related to the above is the question of the source of chelatable lead. It was noted in
Chapter 10 that some sizable fraction of chelatable lead is derived from bone and this compels
reappraisal of the notion that bone is an "inert sink" for otherwise toxic body lead. The no-
tion of bone lead as toxicologically inert never did accord with what was known from studies
of bone physiology, i.e., that bone is a "living" organ, and the thrust of recent studies of
chelatable lead (as well as interrelationships of lead and bone metabolism) is toward bone
lead being viewed as actually an insidious source of long-term systemic lead exposure rather
than a protective mechanism permitting significant lead contact in Industrialized populations.
The complex interrelationships of lead exposure, blood lead, and lead 1n body compart-
ments is of particular Interest in considering the disposition of lead in young children.
Since children take in more lead on a weight basis, and absorb and retain more of this lead
than the adult, one might expect that either tissue and blood levels would be significantly
elevated or that the child's skeletal system would be more efficient in lead sequestration.
Blood lead levels in young children are either similar to adults (males) or somewhat
higher (adult females). Limited autopsy data, furthermore, indicate that soft tissue levels
in children are not markedly different from adults, whereas the skeletal system shows an
approximate 2-fold increase in lead concentration from infancy to adolescence. Neglected 1n
this observation is the fact that the skeletal system In children grows at an exponential
rate, so that skeletal mass increases 40-fold during the interval in childhood when bone lead
levels Increase 2-fold, resulting in an actual increase of approximately 80-fold in total ske-
letal lead. If the skeletal growth factor is taken into account, along with growth in soft
tissue and the expansion of vascular fluid volumes, the question of lead disposition in
children 1s better understood.
Finally, limited animal data Indicate that blood lead alterations with changes in lead
exposure are poor Indicators of such changes in target tissue. Specifically, it appears that
abrupt reduction of lead exposure will be more rapidly reflected 1n blood lead than in such
target tissues as the central nervous system, especially in the developing organism. This
discordance may underlie the observation that severe lead neurotoxicity 1n children is assoc-
iated with a rather broad range of blood lead values (see Section 1.12.4).
The above discussion of some of the problems with the use of blood lead 1n assessing tar-
get tissue burdens or the toxicologically active fraction of total body lead highlights the
the Inherent toxicokinetlc problems with use of blood lead levels 1n defining margins of safe-
ty for avoiding internal lead exposure levels associated with undue risk of adverse effects.
If, for example, blood lead levels of 40-50 ng/dl in "asymptomatic" children are associated
with chelatable lead burdens which overlap those encountered 1n frank pediatric plumblsm, as
documented in one series of lead-exposed children, then there is no margin of safety at these
blood levels for severe effects which are not at all a matter of controversy. Were it both
CHPD1/A 1-133 9/30/83
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PRELIMINARY DRAFT
logistical ly feasible to do so on a large scale and were the use of chelants free of health
risk to the subjects, serial provocative chelation testing would appear to be the better indi-
cator of exposure and risk. Failing this, the only prudent alternative is the use of a large
safety factor applied to blood lead which would translate to an "acceptable" chelatable bur-
den. It is likely that this blood lead value would lie well below the currently accepted up-
per limit of 30 pg/dl, since the safety factor would have to be large enough to protect
against frank plumbism as well as sore subtle health effects seen with non-overt lead intoxi-
cation. This rationale from the standpoint of lead toxicokinetics is in accord also with the
growing data base for dose -effect relationships of lead's effects on heme biosynthesis,
erythropoiesis, and the nervous system in humans as summarized in Sections 1.12.3 and 1.12.4.
The future developement and routine use of in situ mineral tissue testing at time points
concordant with on-going exposure and the comparison of such results with simultaneous blood
lead and chelatable lead measurement would be of significant value in further defining what
level of blood lead is indeed an acceptable upper limit.
1.13.3.3 Proportional Contributions of Lead in Various Media to Blood lead in Human
Populations
The various mathematical descriptions of the relationship of blood lead to lead in indi-
vidual media—air, food, water, dust, soil—were discussed in some detail in Chapter 11 and
summarized concisely in a preceding section (1.11) of this chapter. Using values for lead
intake/content of those media which appear to represent the current exposure picture for human
populations in the U.S., those relationships are further employed in this section to estimate
proportional inputs to total blood lead levels in U.S. populations. Such an exercise is of
help in providing an overall perspective on which routes of exposure are of most significance
in terms of contributions to blood lead levels seen in U.S. populations.
Table 1-16 tabulates the relative direct contributions (in percentages) of air lead to
blood lead at different air-lead levels for calculated typical background levels of lead from
food and water 1n adults. The blood lead contributions from diet are estimated using the
slope 0.02 Mfl/dl Increase 1n blood lead pg/day intake as discussed in Section 1.11.3. In
Table 1-17 are listed direct contributions of air lead to blood lead at varying air lead
levels for children, given calculated typical background levels of blood lead derived from
food and water as per the work of Ryu et al. (1983). Table 1-18 shows relative contributions
of dust/soil to blood lead at varying dust/soil levels for children given calculated back-
ground levels of blood lead from air, food, and water. Assuming that virtually all soil/dust
lead is due to atmospheric fallout of lead particles, the percentage contribution of air lead
directly and indirectly to blood lead becomes significantly greater than when considering just
the direct impact of inhaling lead in the ambient air.
\
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PRELIMINARY DRAFT
TABLE 1-16. DIRECT CONTRIBUTIONS OF AIR LEAO TO BLOOD LEAD (PbB)
IN ADULTS AT FIXED INPUTS OF WATER AND FOOD LEAD
A1r Lead
(pg/n3)
PbB (Air)8
PbB (Food)b
PbB (Water)0
% PbB
From A1r
0.1
0.2
2.0
0.6
7.1
1.0
2.0
2.0
0.6
43.4
1.5
3.0
2.0
0.6
53.5
9 a%UHr= 2-° for 3-2 MB/#3 or less.
^Assuming 100 (jg/day lead from diet and slope 0.02 as discussed in Section 11.4.2.4.
cAssuming 10 yg/i water, Pocock et al. (1983).
TABLE 1-17. DIRECT CONTRIBUTIONS OF AIR LEAD TO BLOOD LEAD IN CHILDREN AT
FIXED INPUTS OF FOOD AND WATER LEAD
Air Lead . _ % PbB
(|jg/m3) PbB (Air) PbB (Food)0 PbB (Water)c Front Air
0.1 0.2 16.0 0.6 1.2
0.5 1.0 16.0 0.6 5.7
1.0 2.0 16.0 0.6 10.8
1.5 3.0 16.0 0.6 15.3
2.5 5.0 16.0 0.6 23.1
' /pblfr= 2,0 for 32 or less.
^Assuming 100 pg Pb/day based upon Ryu et al. (1983).
cAssuaing 10 jjg Pb/1 water, using Pocock et al. (1983).
TABLE 1-18. CONTRIBUTIONS OF DUST/SOIL LEAD TO BLOOD LEAD IN CHILDREN AT
FIXED INPUTS OF AIR, FOOD, AND WATER LEAD
Dust-Soil
Air Lead
PbB a
PbB k
PbB .
PbB .
X PbB
(Mfl/fl)
Mfl/m*
(A1r)
(Food)0
(Water)
(Dust-Soil)
From Dust/Soil
500
0.5
1.0
16.0
0.6
0.3/3.4
1.7/16.2
1000
0.5
1.0
16.0
0.6
0.6/6.8
3.3/27.8
2000
0.5
1.0
16.0
0.6
1.2/13.6
6.4/43.6
* /pt^AIr* 2-° for 3 2 M9/®3 or less.
bAssun1ng 100 jig Pb/day based on Ryu et al. (1983).
cAssum1ng 10 ^9 Pb/1 water, based on Pocock et al. (1983).
dBased on range 0.6 to 6.8 jig/dl for 1000 Mfl/g (Angle and Mclntlre, 1979).
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1.13.4 BIOLOGICAL EFFECTS OF LEAO RELEVANT TO THE GENERAL HUMAN POPULATION
It is clear from the wealth of available literature reviewed in Chapter 12, that there
exists a continuum of biological effects associated with lead across a broad range of expo-
sure. At rather low levels of lead exposure, biochemical changes, e.g., disruption of certain
enzymatic activities involved in heme biosynthesis and erythropoietic pyrimidine metabolism,
are detectable. Heme biosynthesis is a generalized process in mammalian species, including
man, with importance for noma! physiological functioning of virtually all organ systems.
With increasing lead exposure, there are sequentially more intense effects on heme synthesis
and a broadening of lead effects to additional biochemical and physiological mechanisms in
various tissues, such that increasingly more severe disruption of the normal functioning of
many different organ systems becomes apparent. In addition to heme biosynthesis impairment at
relatively low levels of lead exposure, disruption of normal functioning of the erythropoietic
and the nervous systems are among the earliest effects observed as a function of increasing
lead exposure. With increasingly intense exposure, more severe disruption of the erythropoie-
tic and nervous systems occur and additional organ systems are affected so as to result, for
example, 1n the manifestation of renal effects, disruption of reproductive functions, and im-
pairment of immunological functions. At sufficiently high levels of exposure, the damage to
the nervous system and other effects can be severe enough to result in death or, in some cases
of non-fatal lead poisoning, long-lasting sequelae such as permanent mental retardation.
As discussed in Chapter 12 of this document, numerous new studies, reviews, and critiques
concerning Pb-related health effects have been published since the issuance of the earlier EPA
lead criteria document 1n 1977. Of particular importance for present criteria development
purposes are those new findings, taken together with information earlier available at the
writing of the 1977 Criteria Document, which have bearing, on the establishment of quantitative
dose-effect or dose-response relationships for biological effects of lead potentially viewed
as adverse health effects likely to occur among the general population at or near existing
ambient air concentrations of lead in the United States. Key information regarding observed
health effects and their Implications are discussed below for adults and children.
For the latter group, children, emphasis is placed on the discussion of (1) heme biosyn-
thesis effects, (2) certain other biochemical and hematological effects, and (3) the disrup-
tion of nervous system functions. All of these appear to be among those effects of most con-
cern for potential occurrence in association with exposure to existing U.S. ambient air lead
levels of the population group (i.e., children S6 years old) at greatest risk for lead-induced
health effects. Emphasis is also placed on the delineation of internal lead exposure levels,
as defined mainly by blood-lead (PbB) levels, likely associated with the occurrence of such
effects. Also discussed are characteristics of the subject effects that are of crucial impor-
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tance in regard to the determination of which night reasonably be viewed as constituting
"adverse health effects" 1n affected human populations.
1.13.4.1 Criteria for Defining Adverse Health Effects. Over the years, there has been super-
inposed on the continuum of lead-induced biological effects various judgments as to which
specific effects observed in Man constitute "adverse health effects". Such judgments involve
not only medical concensus regarding the health significance of particular effects and their
clinical management, but also incorporate societal value judgments. Such societal value judg-
ments often vary depending upon the specific overall contexts to which they are applied, e.g.,
in judging permissible exposure levels for occupational versus general population exposures to
lead. For some lead exposure effects, e.g., severe nervous system damage resulting In death
or serious medical sequelae consequent to intense lead exposure, there exists little or no
disagreement as to these being significant "adverse health effects." For many other effects
detectable at sequentially lower levels of lead exposure, however, the demarcation lines as to
which effects represent adverse health effects and the lead exposure levels at which they are
accepted as occurring are neither sharp nor fixed, having changed markedly during the past
several decades. That is, from a historical perspective, levels of lead exposure deemed to be
acceptable for either occupationally exposed persons or the general population have been
steadily revised downward as more sophisticated biomedical techniques have revealed formerly
unrecognized biological effects and concern has increased 1n regard to the medical and social
significance of such effects.
It is difficult to provide a definitive statement of all criteria by which specific bio-
logical effects associated with any given agent can be judged to be "adverse health effects".
Nevertheless, several criteria are currently well-accepted as helping to define which effects
should be viewed as "adverse". These include: (1) impaired normal functioning of a specific
tissue or organ system Itself; (2) reduced reserve capacity of that tissue or organ system In
dealing with stress due to other causative agents; (3) the reverslbllity/1rreversibility of
the particular effect(s); and (4) the cumulative or aggregate impact of various effects on
individual organ systems on the overall functioning and well-being of the individual.
Examples of possible uses of such criteria in evaluating lead effects can be cited for
Illustrative purposes. For example, impairment of heme synthesis intensifies with increasing
lead exposure until hemeprotein synthesis is inhibited in many organ systems, leading to re-
ductions in such functions as oxygen transport, cellular energetics, and detoxification of
xenobiotic agents. The latter effect can also be cited as an example of reduced reserve capa-
city pertinent to consideration of effects of lead, the reduced capacity of the liver to deto-
xify certain drugs or other xenobiotic agents resulting from lead effects on hepatic detoxifi-
cation enzyme systems.
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PRELIMINARY DRAFT
In regard to the issue of reversibility/irreversibillty of lead effects, there are really
two dimensions to the issue that need to be considered, i.e.: (1) biological reversibility or
irreversibility characteristic of the particular effect 1n a given organism; and (2) the gene-
rally less-recognized concept of exposure reversibility or irreversibility. Severe central
nervous system damage resulting from intense, high level lead exposure is generally accepted
as an irreversible effect of lead exposure; the reversibility/irreversibility of certain more
difficult-to-detect neurological effects occurring at lower lead exposure levels, however,
remains a matter of some controversy. The concept of exposure reversibility/irreversibillty
can be illustrated by the case of urban children of low socioecomomic status showing dis-
turbances 1n heme biosynthesis and erythropoiesis. Biologically, these various effects may be
considered reversible; the extent to which actual reversibility occurs, however, is determined
by the feasibility of removing these subjects from their particular lead exposure setting. If
such removal from exposure is unlikely or does not occur, then such effects will logically
persist and, defacto, constitute essentially Irreversible effects.
1.13.4.2 Dose-Effect Relationships for Lead-Induced Health Effects
Human Adults. Table 1-19 concisely summarizes the lowest observed effect levels (1n
terms of blood lead concentrations) thus far credibly associated with particular health ef-
fects of concern for human adults in relation to specific organ systems or generalized physio-
logical processes, e.g. heme synthesis.
The most serious effects associated with markedly elevated blood lead levels are severe
neurotoxic effects that include irreversible brain damage as indexed by the occurrence of
acute or chronic encephalopathy symptoms observed 1n both humans and experimental animals.
For most human adults, such damage typically does not occur until blood lead levels exceed
100-120 Often associated with encephalopathic symptoms at such blood lead levels or
higher are severe gastrointestinal symptoms and objective signs of effects on several other
organ systems as well. The precise threshold for occurrence of overt neurological and gastro-
intestinal signs and symptoms of lead intoxication remains to be established but such effects
have been observed in adult lead workers at blood lead levels as low as 40-60 jjg/d1, notably
lower than the 60 or 80 \iQ/4"\ levels previously established or. discussed as being "safe" for
occupational lead exposure.
Other types of health effects occur coincident with the above overt neurological and gas-
trointestinal symptoms indicative of marked lead intoxication. These range from frank peri-
pheral neuropathies to chronic renal nephropathy and anemia. Toward the lower range of blood
lead levels associated with overt lead intoxication or somewhat below, less severe but impor-
tant signs of Impairment 1n normal physiological functioning 1n several organ systems are
evident, including: (1) slowed nerve conduction velocities indicative of peripheral nerve
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TABU 1-19. SUMMARY OF LOWEST OBSERVED EFFECT LEVELS FOR KEY LEAD-INDUCED HEALTH EFFECTS IN ADULTS
lowest Observed
Effect Level (Mj8)
Hom Synthesis ami
Hematological Effects
Neurological
Effects
Renal Systea
Effects
Reproductive
Function Effects
Gastrointestinal
Effect*
100-120 pg/dl
80 pg/dl
60 pg/dl
50 MO/dl
W
10
40 tig/dl
30 pg/dl
25-30 pg/dl
15-20 Mfl/dl
<10 pg/dl
Frank imfa
Reduced hemoglobin
production
Increased urinary ALA and
elevated coproporphyria
Erythrocyte protoporphyrin
(EP) elevation In Mies
Erythrocyte protoporphyrin
(EP) elevation In feaales
ALA-0 Inhibition
Encephalopathy signs
and syaptOK
T.
Overt subenctphal opathl c
neurological syaptoas
1'
Peripheral nerve dysfunction
(slowed nerve conduction)
Chronic renal
nephropathy
N
Overt gastrointestinal
syaptoas (colic, etc.)
Altered testicular
ctlon
fun|t1
Abbreviations: Pb6 = blood lead concentrations.
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PRELIMINARY DRAFT
dysfunction (at 30-40 pg/dl, or possibly lower levels); (2) altered testicular function (at
40-50 Mfl/dl); and (3) reduced hemoglobin production (at approximately 50 pg/dl) and other
signs of impaired heme synthesis evident at still lower blood lead levels. All of these ef-
fects point toward a generalized impairment of normal physiological functioning across several
different organ systems, which becomes abundantly evident as adult blood lead levels approach
or exceed 30-40 (jg/dl. Evidence for Impaired heme synthesis effects in blood cells exists at
still lower blood lead levels in human adults and the significance of this and evidence of
impairment of other biochemical processes Important in cellular energetics are the subject of
discussion below in relation to health effects observed in children.
Children. Table 1-20 summariies lowest observed effect levels for a variety of imporatnt
health effects observed in children. Again, as for adults, it can be seen that lead impacts
many different organ systems and biochemical/physiological processes across a wide range of
exposure levels. Also, again, the most serious of these effects is the severe, irreversible
central nervous system damage manifested in terms of encephalopathic signs and symptoms. In
children, effective blood lead levels for producing encephalopathy or death are lower than for
adults, starting at approximately 80-100 pg/dl. Other overt neurological symptoms are evident
at somewhat lower blood lead levels associated with lasting neurological sequalae. Colic and
other overt gastrointestinal symptoms clearly occur at similar or still lower blood lead
levels in children, at least down to 60 jjg/dl and, perhaps, below. Renal dysfunction is also
manifested along with the above overt signs of lead intoxication in children and has been
reported at blood lead levels as low as 40 MS/dl in some pediatric populations. Frank anemia
is also evident at 70 yg/dl, representing an extreme manifestation of reduced hemoglobin syn-
thesis observed at blood lead levels as low as 40 MS/dl along with other signs of marked heme
synthesis inhibition at that exposure level. Again, all of these effects are reflective of
widespread impact of lead on the normal physiological functioning of many different organ
systems in children at blood lead levels at least as low as 40 ng/dl.
Among the most important and controversial of the issues discussed 1n Chapter 12 are the
evaluation of neuropsychological or electrophysiological effects associated with low-level
lead exposures 1n non-overtly lead intoxicated children. None of the available studies on the
subject, individually, can be said to prove conclusively that significant neurological effects
occur in children at blood-Pb levels <30 yg/dl. The collective neurobehavloral studies of CNS
{cognitive; IQ) effects, for example, can probably now be most reasonably interpreted as most
clearly being indicative of a likely association between neuropsychologic deficits and low-
level Pb-exposures in young children resulting in blood-Pb levels of approximately 30 to 50
yg/dl. However, due to specific methodological problems with each of the various studies (as
noted in Chapter 12), much caution is warranted that precludes conclusive acceptance of the
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TABLE 1-20. SifVMRY OF LOWEST OBSERVED EFFECT LEVELS FOR KEY LEAO-INDUCEO HEALTH EFFECTS IN CHILDREN
Lowest Observed
Effect Level (PbB)
Heat Synthesis ami
Hematological Effects
Neurological
Effects
Renal Systee
Effects
Gastrointestinal
Effects
Other Biochemical
Effects
80-100 |ig/d!
70 i*9/d1
60 M9/0)
50 yg/dl
t
£ 40 Mfl/dt
30 |>0/41
15-20 pg/dl
10
Frank anemia
Reduced hemoglobin
Elevated coproporphyrin
Increased urinary ALA
Erythrocyte protoporphyin
elevatton
ALA-D Inhibition
Encephalopathy
signs and symptoms
I
Cognitive (CMS) deflcts
Peripheral nerve dysfunction
(slowed NCV's)
CNS electrophysiological
deficits
4
?
Renal dys-
function
(aminoaciduria)
Colic, other overt
gastrointestinal symptoms
Vitamin 0 metabolism
Interference
Py-5-N activity
Inhibition
Abbreviations: PbB = blood lead concentrations; Py-5-N = pyrimidine-5'-nucleotidase.
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PRELIMINARY DRAFT
observed effects being due to Pb rather than other (at times uncontrolled for) potentially
confounding variables.
Also of considerable importance are studies by which provide evidence of changes in EEG
brain wave patterns and CNS evoked potential responses In non-overtly lead Intoxicated chil-
dren experiencing relatively low blood-Pb levels. Sufficient exposure information was pro-
vided by these studies and appropriate statistical analyses were carried out which demonstra-
ted clear, statistically significant associations between electrophysiological (SW voltage)
changes and blood-Pb levels in the range of 30 to 55 pg/dl and probable analogous associations
at blood-Pb levels below 30 yg/dl (with no evident threshold down to 15 jjg/dl). In this case,
the continued presence of such electrophysiological changes upon follow-up two years later,
suggests persistence of such effects even in the face of later declines in blood-Pb levels
and, therefore, possible non-reversibility of the observed electrophysiological CNS changes.
However, the reported electrophysiological effects were not found to be significantly assoc-
iated with IQ decrements.
The precise medical or health significance of the neuropsychological and electrophysiolo-
gical effects found by the above studies to be associated with low-level Pb-exposures is dif-
ficult to state with confidence at this time. The IQ deficits and other behavioral changes,
although statistically significant, are generally relatively small in magnitude as detected by
the reviewed studies, but nevertheless may still impact the intellectual development, school
performance, and social development of the affected children sufficiently so as to be regarded
as adverse. This would be especially true if such impaired Intellectual development or school
performance and disrupted social development were reflective of persisting, long-term effects
of low-level lead exposure in early childhood. The issue of persistence of such lead effects,
however, remains to be more clearly resolved, with some study results reviewed in Chapter 12
and mentioned above suggesting that significant low-level Pb-induced neurobehavioral and EEG
effects may, in fact, persist into later childhood.
In regard to additional studies reviewed in Chapter 12 concerning the neurotoxicity of
lead, certain evidence exists which suggests that neurotoxic effects may be associated with
lead-induced altered heme synthesis, which results in an accumulation of ALA in brain affec-
ting CNS GABA synthesis, binding, and/or inactivation by neuronal reuptake after synaptic
release. Also, available experimental data suggest that these effects may have functional
significance in the terms of this constituting one mechanism by which lead may increase the
sensitivity of rats to drug-induced seizures and, possibly, by which GABA-related behavioral
or physiological control functions are disrupted. Unfortunately, the available research data
do not allow credible direct estimates of blood-lead levels at which such effects might occur
in rats, other non-human mammalian species, or man. Inferentially, however, one can state
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that threshold levels for any marked lead-Induced ALA impact on CNS GA8A mechanisms are most
probably at least as high as blood-lead levels at which significant accumulations of ALA have
been detected in erythrocytes or non-blood soft tissues (see below). Regardless of any dose-
effect levels inferred, though, the functional and/or medical significance of lead-induced ALA
effects on CNS mechanisms at low-levels of lead-exposure remains to be more fully determined
and cannot, at this time, be unequivocably seen as an adverse health effect.
Research concerning lead-induced effects on heme synthesis, also provides information of
importance in evaluating whether significant health effects in children are associated with
blood-lead levels below 30 pg/dl. As discussed earlier, lead affects heme synthesis at
several points in its metabolic pathway, with consequent impact on the normal functioning of
many body tissues. The activity of the enzyme, ALA-S, catalyzing the rate-limiting step of
heme synthesis does not appear to be significantly affected until blood-lead levels reach or
exceed approximately 40 pg/dl. The enzyme ALA-D, which catalizes the conversion of ALA to
porphobilinogen as a further step in the heme biosynthetic pathway, appears to be affected at
much lower blood-lead levels as indexed directly by observations of ALA-D inhibition or indi-
rectly in terms of consequent accumulations of ALA in blood and non-blood tissues. More
specifically, inhibition of erythrocyte ALA-D activity has been observed in humans and other
mammalian species at blood-lead levels even below 10 to 15 \ig/dl, with no clear threshold evi-
dent. Correlations between erythrocyte, and hepatic ALA-D activity inhibition in lead workers
at blood-lead levels in the range of 12 to 56 pg/dl suggest that ALA-D activity in soft tis-
sues (eg. brain, liver, kidney, etc.) may be inhibited at similar blood-lead levels at which
erythrocyte ALA-D activity inhibition occurs, resulting in accumulations of ALA in both blood
and soft tissues.
It is now clear that significant increases In both blood and urinary ALA occur below the
currently commonly-accepted blood-lead level of 40 Mfl/dl and, in fact, such increases in blood
and urinary ALA are detectable in humans at blood-lead levels below 30 iig/dl, with no clear
threshold evident down to 15 to 20 pg/dl. Other studies have demonstrated significant eleva-
tions in rat brain, spleen and kidney ALA levels consequent to acute or chronic lead-exposure,
but no clear blood-lead levels can yet be specified at which such non-blood tissue ALA in-
creases occur in humans. It is reasonable to assume, however, that ALA increases in non-blood
tissues likely begin to occur at roughly the same blood-lead levels associated with increases
in erythrocyte ALA levels.
Lead also affects heme synthesis beyond metabolic steps involving ALA, leading to the
accumulation of protoporphyrin in erythrocytes as the result of impaired iron insertion Into
the porphyrin moiety to form heme. The porphyrin acquires a zinc ion in lieu of the native
iron, and the resulting accumulation of blood zinc protoporphyrin (ZPP) tightly bound to ery-
throcytes for their entire life (120 days) represents a commonly employed index of lead-
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PRELIMINARY DRAFT
exposure for medical screening purposes. The threshold for elevation of erythrocyte protopor-
phyrin (EP) levels is well-established as being 25 to 30 pg/dl in adults and approximately 15
fjg/dl for young children, with significant EP elevations (>1 to 2 standard deviations above
reference noma! EP mean levels) occurring in 50 percent of all children studied as blood-lead
levels approach or moderately exceed 30 pg/dl•
Medically, small increases in EP levels have generally not been viewed as being of great
concern at initial detection levels around 15 to 20 jjg/dl in children, but EP increases become
more worrisome as markedly greater, significant EP elevations occur as blood-lead levels
approach and exceed 30 pg/dl and additional signs of significantly deranged heme synthesis
begin to appear along with indications of functional disruption of various organ systems.
Previously, such other signs of significant organ system functional disruptions had only been
credibly detected at blood-lead levels somewhat in excess of 30 (jg/dl, e.g., hemoglobin syn-
thesis inhibition starting at 40 Mfl/dl and significant nervous system effects at 50-60 Mg/dl.
This served as a basis for CDC establishment of 30 yg/dl blood-lead as a criteria level for
undue lead exposure for young children and adoption by EPA of it as the "maximum safe" blood-
lead level (allowing some margin.of safety before reaching levels associated with inhibition
of hemoglobin synthesis or nervous system deficits) in setting the 1978 NAAQS for lead.
To the extent that new evidence is now available, indicative of probable lead effects on
nervous system functioning or other important physiological processes at blood-lead levels
below 30 to 40 Mfl/dl, then the rationale for continuing to view 30 yg/dl as a "maximum safe"
blood-lead level is called into question and substantial impetus is provided for revising the
criteria level downward, i.e., to some blood-lead level below 30 jjg/dl. At this time, such
impetus toward revising the blood-lead criteria level downward is gaining momentum not only
from new neuropsychologic and electrophysiological findings of the type summarized above, but
also from growing evidence for lead effects on other functional systems. These include, for
example, the: (1) disruption of formation of the heme-containing protein, cytochrome c, of
considerable importance in cellular energetics involved in mediation of the normal functioning
of many different mammalian (including human) organ systems and tissues; (2) inhibition by
lead of the biosynthesis of globln, the protein moiety of hemoglobin, 1n the presense of lead
at concentrations corresponding to a blood-lead level of 20 jjg/dlj (3) observations of signi-
ficant inhibition of pyrimidine-5'-nucleotidase (Py-5-N) activity in adults at blood-lead
levels 244 pg/dl and in children down to blood-lead levels of 10 yg/dl; and (4) observations
of lead interference with vitamin 0 metabolism in children across a blood-lead level range of
33 to 120 Mg/dl, with consequent increasingly enhanced lead uptake due to decreased vitamin 0
metabolism and likely associated Increasingly cascading effects on nervous system and other
functions at sequentially higher blood-lead levels. Certain additional evidence for lead ef-
fects on hormonal systems and immune system components, thus far detected only at relatively
CHPDl/A 1-144 9/30/83
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PRELIMINARY DRAFT
high blood-lead levels or at least not credibly associated with blood-lead levels as low as 30
to 40 Mfl/dl, also contributes to concern as blood-lead levels exceed 30 pg/dl.
Also adding to the concern about relatively low lead exposure levels are the results of
an expanding array of animal toxicology studies which demonstrate: (1) persistence of lead-
Induced neurobehavloral alterations well Into adulthood long after termination of perinatal
lead exposure early In development of several mammalian species; (2) evidence for uptake and
retention of lead in neural and non-neuronal elements of the CNS, including long-term persis-
tence 1n brain tissues after termination of external lead exposure and blood lead levels
return to "normal"; and (3) evidence from various in-vivo and 1n-vitro studies Indicating
that, at least on a subcellular-molecular level, no threshold m^y exist for certain neurochem-
ical effects of lead.
1.13.5 DOSE-RESPONSE RELATIONSHIPS FOR LEAD EFFECTS IN HUMAN POPULATIONS
Information summarized in the preceding section dealt with the various biological effects
of lead germane to the general population and included comments about the various levels of
blood lead observed to be associated with the measurable onset of these effects in various
populations groups.
A number of Investigators have attempted to quantify more precisely dose-population
response relationships for some of the above lead effects in human populations. That is they
have attempted to define the proportion of a population exhibiting a particular effect at a
given blood lead level. To date, such efforts at defining dose-response relationships for
lead effects have been mainly limited to the following effects of lead on heme biosynthesis:
inhibition of ALA-D activity; elevation of EP; and urinary excretion of ALA.
Dose-population response relationships for EP in children has been analyzed 1n detail by
Piomelli and et al. (1982) and the corresponding plot at 2 levels of elevation (>1 S.D., >2
S.D.) is shown in Figure 1-19 using problt analysis. It can be seen that blood lead levels in
half of the children showing EP elevations at >1 and 2 S.D.'s closely bracket the blood lead
level taken as the high end of "normal" (i.e., 30 pg/dl). Dose-response curves for adult men
and women as well as children prepared by Roels et al. (1976) are set forth in Figure 1-20.
In Figure 1-20, it may be seen that the dose-response for children remains greater across the
blood-lead range studied, followed by women, then adult males.
Figure 1-21 presents dose-population response data for urinary ALA exceeding two levels
(at mean + 1 S.D. and mean + 2 S.O.), as calculated by EPA from the data of Azar et at.
(1975). The percentages of the study populations exceeding the corresponding cut-off levels
as calculated by EPA for the Azar data are set forth In Table 1-21. It should be noted that
the measurement of ALA 1n the Azar et al. study did not account for amino acetone, which nay
Influence the results observed at the lowest blood lead levels.
CHPD1/A 1-145 9/30/83
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PRELIMINARY ORAFT
3
<
D
a
z
S
5
S
§
£
NATURAL FREQUENCY _
10
20
30
40
ao
70
BO
BLOOO LEAD. moMI
Hgure 1-19. Do— response for elevation of EP sa a
function of blood load level using probtt analyals.
Geometric mean plus 1 3-D. * 33 tigldl; geometric mean
plus 2 S.D. - 63 pg/dl.
Source: Piomelli at el. (1882).
100
FEP
I
A
AOULT FEMALES
CHILDREN /'/
41
Z
1
2
2
it.
o
ADULT MALES
1
o
10
20
30
40
SO
BLOOD LEAD LEVEL. |« PUdi
Figure 1-20. Doee-rasponoe curve for FEP as a function
of blood lead level: In aubpopuiattona.
Source: Roels et al. (1978).
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PRELIMINARY DRAFT
3
100
a
I
A
3
3
<
90
80
70
00
3
2
s
u.
0
Uf
1
iy
U
5
a
40
30
20
10
O MEAN + 1 S.D.
A MEAN + 2 8.D.
MEAN ALAU - 0.32 FOR
BLOOD LEAD< 13 pg/dl
10 20 30 40 BO 60 70 80 90
BLOOD LEAD LEVEL Pb/dl
Figure 1-21. EPA calculated do«e-re*ponse curve for
ALA-U.
Source: Azar et al. (1975).
TABLE 1-21. EPA-ESTIMATED PERCENTAGE OF SUBJECTS
WITH ALA-U EXCEEDING LIMITS FOR VARIOUS BLOOD LEA0 LEVELS
Blood lead levels Azar et al. (1975)
(pg/dl) (Percent Population)
10 2
20 6
30 16
40 31
50 50
60 69
70 84
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PRELIMINARY DRAFT
1.13,6 POPULATIONS AT RISK
Population at risk is a segment of a defined population exhibiting characteristics asso-
ciated with significantly higher probability of developing a condition, illness, or other ab-
normal status. This high risk may result from either (1) greater inherent susceptibility or
(2) from exposure situations peculiar to that group. What is meant by inherent susceptibility
is a host characteristic or status that predisposes the host to a greater risk of heightened
response to an external stimulus or agent.
In regard to lead, two such populations are definable. They are preschool age children,
especially those living in urban settings, and pregnant women, the latter group owing mainly
to the risk to the conceptus. Children are such a population for both of the reasons stated
above, whereas pregnant women are at risk primarily due to the inherent susceptibility of the
conceptus.
1.13.6.1 Children as a Population at Risk. Children are developing and growing organisms ex-
hibiting certain differences from adults in terms of basic physiologic mechanisms, capability
of coping with physiologic stress, and their relative metabolism of lead. Also, the behavior
of children frequently places them in different relationship to sources of lead in the envi-
ronment, thereby enhancing the opportunity for them to absorb lead. Furthermore, the occur-
rence of excessive exposure often is not realized until serious harm is done. Young children
do not readily communicate a medical history of lead exposure, the early signs of such being
common to so many other disease states that lead is frequently not recognized early on as a
possible etiological factor contributing to the manifestation of other symptoms.
Inherent Susceptibility of the Young. Discussion of the physiological vulnerability of
the young must address two discrete areas. Not only should the basic physiological differ-
ences be considered that one would expect to predispose children to a heightened vulnerability
to lead, but also the actual clinical evidence must be considered that shows such vulnerabil-
ity does indeed exist.
In Chapter 10 and Section 1.13.2 above, differences in relative exposure to lead and body
handling of lead for children versus adults were pinpointed throughout the text. The signifi-
cant elements of difference Include: (1) greater intake of lead by Infants and young children
Into the respiratory and gastro-intestinal tracts on a body weight basis compared to adults;
(2) greater absorption and retention rates of lead In children; (3) much greater prevalence of
nutrient deficiency in the case of nutrients which affect lead absorption rates from the GI
tract; (4) differences in certain habits, i.e., normal hand to mouth activity as well as pica
resulting In the transfer of lead-contaminated dust and dirt to the GI tract; (5) differences
1n the efficiency of lead sequestration in the bones of children, such that not only is less
of the bocfy burden of lead in bone at any given time but the amount present may be relatively
¦ore labile. Additional information discussed in Chapter 12 suggests that the blood-brain
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PRELIMINARY DRAFT
barrier in children is less developed, posing the risk for greater entry of lead Into the
nervous system.
Hematological and neurological effects in children have been demonstrated to have lower
thresholds in terms of blood lead levels than in adults. The extent of reduced hemoglobin
production and EP accumulation occur at relatively lower exposure levels in children than in
adults, as indexed by blood lead thresholds. With reference to neurologic effects, the onset
of encephalopathy and other injury to the nervous system appears to vary both regarding likely
lower thresholds in children for some effects and in the typical pattern of neurologic effects
presented, e.g., in encephalopathy or other CNS deficits being more common in children versus
peripheral neuropathy being more often seen in adults. Not only are the effects more acute in
children than in adults, but also the neurologic sequelae are usually much more severe 1n
children.
Exposure Consideration. The dietary habits of children as well as the diets themselves
differ markedly from adults and, as a result, place children In a different relationship to
several sources of lead. The dominance of canned milk and processed baby food in the diet of
•any young children is an important factor 1n assessing their exposure to lead since both
those foodstuffs have been shown to contain higher amounts of lead than components of the
adult diet. The importance of these lead sources is not their relationship to airborne lead
directly but, rather, their role 1n providing a higher baseline lead burden to which the air-
borne contribution is added.
Children ordinarily undergo a stage of development in which they exhibit normal mouthing
behavior, as manifested, for example, in the form of thumbsucking. At this time they are at
risk for picking up lead-contaminated soil and dust on their hands and hence into their mouths
where it can be absorbed. Scientific evidence documenting at least the first part of the
chain is available.
There is, however, an abnormal extension of mouthing behavior, called pica, which occurs
in some children. Although diagnosis of this is difficult, children who exhibit this trait
have been shown to purposefully eat nonfood items. Much of the lead-based paint problem 1s
known to occur because children actively Ingest chips- of leaded paint.
1.13.6.2 Pregnant Women and the Conceptus as a Population at Risk. There are some rather in-
conculsive data indicating that women may In general be somewhat higher risk to lead than men.
However, pregnant women and their concepti as a subgroup are demonstrably at higher risk. It
should be pointed out that, in fact, it really is not the pregnant woman ger se who 1s at
greatest risk but, rather, the unborn child she is carrying. Because of obstetric complica-
tions, however, the mother herself can also be at somewhat greater risk at the time of deliv-
ery of her child.
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Studies have demonstrated that women in general, like children, tend to show a heightened
response of erythorcyte protoporphyrin levels upon exposure to lead. The exact reason for
this heightened response is not known but may relate to endocrine differences between men and
women.
As stated above, the primary reason pregnant women are a high-risk group is because of
the fetus each is carrying. In addition, there is some suggestive evidence that lead expo-
sures may also affect maternal complications at delivery. With reference to maternal compli-
cation at delivery, information in the literature suggests that the incidence of preterm deli-
very and premature membrane rupture relates to maternal blood lead level. Further study of
this relationship as well as studies relating to discrete health effects in the newborn are
needed.
Vulnerability of the developing fetus to lead exposure arising from transplacental trans-
fer of maternal lead was discussed in Chapter 10. This process starts at the end of the first
trimester. Umbilical cord blood studies involving mother-infant pairs have repeatedly shown a
correlation between maternal and fetal blood lead levels.
Further suggestive evidence, cited in Chapter 12, has been advanced for prenatal lead
exposures of fetuses possibly leading to later higher instances of postnatal mental retarda-
tion among the affected offspring. The available data are insufficient to state with any cer-
tainty that such effects occur or to determine with any precision what levels of lead exposure
might be required prior to or during pregnancy in order to produce such effects.
1.13.6.3 Description of the United States Population in Relation to Potential Lead Exposure
Risk —
In this section, estimates are provided of the number of individuals in those segments of
the population which have been defined as being potentially at greatest risk for lead ex-
posures. These segments include pre-school children (up to 6 years of age), especially those
living in urban settings, and women of child-bearing age (defined here as ages 15-44). These
data, which are presented below in Table 1-22, were obtained from a provisional report by the
U.S. Census Bureau (1982), which indicates that approximately 61 percent of the populace lives
in urban areas (defined as central cities and urban fringe). Assuming that the 61 percent
estimate for urban residents also applies to children of preschool age, then approximately
14,206,000 children of the total listed in Table 1-22 would be expected to be at greater risk
by virtue of higher lead exposures generally associated with their living in urban versus non-
urban settings. (NOTE: The age distribution of the percentage of urban residents nay vary
between SMSA's.)
The risk encountered with exposure to lead may be compounded by nutritional deficits (see
Chapter 10). The most commonly seen of these is iron deficiency, especially in young children
less than 5 years of age (Mahaffey and Michael son, 1980). Data available from the National
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TABLE 1-22. PROVISIONAL ESTIMATE OF THE NUMBER OF INDIVIDUALS IN URBAN AND
RURAL POPULATION SEGMENTS AT GREATEST POTENTIAL RISK TO LEAD EXPOSURE
Population Segment
Actual Age
(year)
Total Number in U.S.
Population
(1981)
Urban
Population1
Pre-school children
0-4
16,939,000
10,333,000
5
3,201,000
1,953,000
6
3,147,000
1.920.000
Total
14,206,000
Women of
15-19
10,015,000
6,109,000
child-bearing age
20-24
10,818,000
6,599,000
25-29
10,072,000
6,144,000
30-34
9,463,000
5,772,000
35-39
7,320,000
4,465,000
40-44
6f147f000
3.749.000
Total
53,835,000
32 838 000
Source: U.S. Census Bureau (1982), Tables 18 and 31.
*An urban/total ratio of 0.61 was used for all age groups. "Urban" Includes central city
and urban fringe populations.
Center for Health Statistics for 1976-1980 (Fulwood et al., 1982) indicate that from 8 to 22
percent of children aged 3-5 may exhibit iron deficiency, depending upon whether this condi-
tion is defined as serum iron concentration (<40 Mfl/dl) or as transferrin saturation (<16 per-
cent), respectively. Hence, of the 20,140,000 children 55 years of age (Table 1-22), as many
as 4,431,000 would be expected to be at increased risk depending on their exposure to lead,
due to iron deficiency.
As pointed out in Section 1.13.7, the risk to pregnant women is mainly due to risk to the
conceptus. By dividing the total number of women of child-bearing age in 1981 (53,835,000)
into the total number of live births in 1981 (3,646,000; National Center for Health Statis-
tics, 1982), it may be seen that approximately 7 percent of this segment of the population
¦ay be at increased risk at any given time.
1.13.7 SUMMARY AN0 CONCLUSIONS
Among the most significant pieces of information and conclusions that emerge from the
present human health risk evaluation are the following;
(1) Anthropogenic activity has clearly led to vast increases of lead input Into those en-
vironmental compartments which serve as media (e.g., air, water, food, etc.) by which
significant human exposure to lead occurs.
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(2) Emission of lead into the atmosphere, especially through leaded gasoline combustion, is
of major significance in terms of both the movement of lead to other environmental com-
partments and the relative impact of such emissions on the internal lead burdens in in-
dustrialized human populations. By means of both mathematical modeling of available
clinical/epidemiological data by EPA and the isotopic tracing of lead from gasoline to
the atmosphere to human blood of exposed populations, the size of atmospheric lead con-
tribution can be confidently said to be 25-50 percent or, probably somewhat higher.
(3) Given this magnitude of relative contribution to human external and internal exposure,
reduction in levels of atmospheric lead would then result in significant widespread
reductions in levels of lead in human blood (an outcome which 1s supported by careful
analysis of the NHANES II study data). Reduction of lead in food (added in the course of
harvesting, transport, and processing) would also be expected to produce significant
widespread reductions in human blood lead levels in the United States.
(~) A number of adverse effects in humans and other species are clearly associated with lead
exposure and, from a historical perspective, the observed "thresholds" for these various
effects (particularly neurological and heme biosynthesis effects) continue to decline as
¦ore sophisticated experimental and clinical measures are employed to detect more subtle,
but still significant effects. These include significant alterations in normal physio-
logical functions at blood lead levels markedly below the currently accepted 30 pg/dl
"maxim safe level" for pediatric exposures.
(5) Several chapters of this document demonstrate that young children Are at greatest risk
for experiencing lead-induced health effects, particularly in the urbanized, low income
segments of this pediatric population. A second group at increased risk are pregnant
women, because of exposure of the fetus to lead in the absence of any effective biologi-
cal (e.g. placental) barrier during gestation.
(6) Dose-population response information for heme synthesis effects, coupled with information
from various blood lead surveys, e.g. the NHANES II study, indicate that large numbers of
American children (especially low income, urban dwellers) have blood lead levels suffi-
ciently high (in excess of 15-20 pg/dl) that they are clearly at risk for deranged heme
synthesis and, possibly, other health effects of growing concern as lead's role as a
general systemic toxicant becomes more fully understood.
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Vostal, J. J.; Taves, E.; Sayre, J. W.; Charney, E. (1974) Lead analysis of the house dust: a
method for the detection of another source of lead exposure in Inner city children.
Environ. Health Perspect. 7; 91-97.
Wai, C. N.; Knowles, C. R.; Keely, J. F. (1979) Lead caps on w1ne bottles and their potential
problems. Bull. Environ. Contain. Toxicol. 21: 4-6.
Walter, S. 0.; Yankel, A. J.; von Lindern, I. H. (1980) Age-specific risk factors for lead
absorption in children. Arch. Environ. Health 35: 53-58.
Watson, W. N.; Witherell, L. E.; Giguere, G. C. (1978) Increased lead absorption in children
of workers in a lead storage battery plant. J. Occup. Med. 20: 759-761.
Wheeler, G. L.; Rolfe, G. L. (1979) The relationship between daily traffic volume and the dis-
tribution of lead In roadside soil and vegetation. Environ. Pollut. 18: 265-274.
Whitby, K. T.; Clark, W. E.; Marple, V. A.; Sverdrup, G. M.; Sem, G. J.; Willeke, K.; -Liu, B.
Y. H.; Pui, D. Y. H. (1975) Characterization of California aerosols-I: size distributions
of freeway aerosol. Atmos. Environ. 9: 463-482.
Williams, M. W.; Turner, J. E. (1981) Comments on softness parameters and metal ion toxicity.
J. Inorg. Nucl. Chem. 43: 1689-1691.
~
Williams, M. W.; Hoescbele, J. D.; Turner, J. E.; Jacobson, K. B.; Christie, N. T.; Paton, C.
L,; Smith, L. H.; Witsch, H. R.; Lee, E. H. (1982) Chemical softness and acute metal
toxicity in mice and Drosophila. Toxicol. Appl. Pharmacol. 63: 461-469.
Williamson, P. (1979) Comparison of metal levels In invertebrate detritivores and their
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Williamson, P. (1980) Variables affecting body burdens of lead, zinc and cadmium In a roadside
population of the snail Cepaea hortensis MUller. Oecologia 44: 213-220.
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Bull. Environ. Contam. Toxicol. 8: 280-288.
01REF/D
1-168
9/30/83
-------
PRELIMINARY DRAFT
Wolnlk, K. A.; Frlcke, F. L.; Capar, S. G.; Braude, 6. L.; Mayer, M. W.; Satzger, R. 0.;
Bonnin, E. (1983) Elements 1n major raw agricultural crops 1ri the United States. I:
Cadmium and lead 1n lettuce, peanuts, potatoes, soybeans, sweet corn and wheat. J.
Agric. Food Chem. (in press)
Wong, M. H. (1982) Metal cotolerance to copper, lead and zinc in Festuca rubra. Environ. Res.
29: 42-47.
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Lead in drinking water: the contribution of household tap water to blood lead levels.
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lationship of childhood lead poisoning and environmental exposure. J. Air Pollut. Control
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Yocum, J. E. (1982) Indoor-outdoor air quality relationships: a critical review. J. Air
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Zimdahl, R. L. (1976) Entry and movement in vegetation of lead derived from air and soil
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1202-1207.
01REF/D 1-169 9/30/83
I • m>.024/l004
-------
3ER&
United States
Environmental Protection
Agency
Environmental Criteria and
Assessment Office
Research Triangle Park NC 27711
CQA6-
.*•/
EPA-600/8-83-028A
August 1983
External Review Draft
Research and Development
Air Quality
Criteria for Lead
Volume II of IV
Review
Draft
(Do Not
Cite or Quote)
NOTICE
This document is a preliminary draft. It has not been formally
released by EPA and should not at this stage be construed to
represent Agency policy. It is being circulated for comment on its
technical accuracy and policy implications.
-------
Draft
Do Not Quote or Cite
EPA-600/8-83-028A
August 1983
External Review Draft
Air Quality Criteria
for Lead
Volume II of IV
NOTICE
This document is a preliminary draft. It has not been formally released by EPA and should not at this stage
be construed to represent Agency policy. It is being circulated for comment on its technical accuracy and
policy implications.
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
-------
ABSTRACT
The document evaluates and assesses scientific information on the health
and welfare effects associated with exposure to various concentrations of lead
in ambient air. The literature through 1983 has been reviewed thoroughly for
information relevant to air quality criteria, although the document is not
intended as a complete and detailed review of all literature pertaining to
lead. An attempt has been made to identify the major discrepancies in our
current knowledge and understanding of the effects of these pollutants.
Although this document is principally concerned with the health and
welfare effects of lead, other scientific data are presented and evaluated in
order to provide a better understanding of this pollutant in the environment.
To this end, the document includes chapters that discuss the chemistry and
physics of the pollutant; analytical techniques; sources, and types of
emissions; environmental concentrations and exposure levels; atmospheric
chemistry and dispersion modeling; effects on vegetation; and respiratory,
physiological, toxicological, clinical, and epidemiological aspects of human
exposure.
111
-------
PRELIMINARY DRAFT
LIST OF TABLES
Table Page
3-1 Properties of elemental lead 3-2
4-1 Design of national air monitoring stations 4-3
4-2 TSP NAMS criteria 4-4
4-3 Description of spatial scales of representativeness 4-7
4-4 Relationship between monitoring objectives and
appropriate spatial scales 4-7
5-1 U.S. utilization of lead by product category 5-6
5-2 Estimated atmospheric lead emissions for the U.S., 1981, and the world —... 5-8
5-3 Light-duty vehicular particulate emissions 5-11
5-4 Heavy-duty vehicular particulate emissions 5-11
5-5 Recent and projected consumption of gasoline lead 5-12
6-1 Summary of microscale concentrations 6-5
6-2 Enrichment of atmospheric aerosols over crustal abundance 6-15
6-3 Comparison of size distributions of lead-containing particles in
major sampling areas 6-21
6-4 Distribution of lead in two size fractions at several sites
in the United States 6-22
6-5 Summary of surrogate and vegetation surface deposition of lead 6-29
6-6 Deposition of lead at the Walker Branch Watershed, 1974 6-31
6-7 Estimated global deposition of atmospheric lead 6-32
7-1 Atmospheric lead in urban, rural and remote areas of the world 7-4
7-2 Cumulative frequency distributions of urban air lead concentrations 7-7
7-3 Air lead concentrations in major metropolitan areas 7-9
7-4 Stations with air lead concentrations greater than 1.0 pg/m3 7-14
7-5 Distribution of air lead concentrations by type of site 7-19
7-6 Vertical distribution of lead concentrations 7-22
7-7 Comparison of indoor and outdoor airborne lead concentrations 7-25
7-8 Summary of soil lead concentrations 7-28
7-9 Background lead in basic food crops and meats 7-28
7-10 Summary of lead in drinking water supplies 7-35
7-11 Summary of environmental concentrations of lead 7-35
7-12 Summary of inhaled air lead exposure 7-39
7-13 Lead concentrations in milk and foods 7-41
7-14 Addition of lead to food products 7-43
7-15 Prehistoric and modern concentrations in human food from a marine food
chain 7-44
7-16 Recent trends of lead concentrations In food items 7-45
7-17 Summary of lead concentrations in milk and foods by source 7-46
7-18 Summary by age and sex of estimated average levels of lead injested from
milk and foods 7-47
7-19 Summary by source of lead consumed from milk and foods 7-50
7-20 Summary.by source of lead concentrations in water and beverages 7-51
7-21 Daily consumption and potential lead exposure from water and beverages 7-52
7-22 Summary by source of lead consumed in water and beverages 7-53
7-23 Current baseline estimates of potential human exposure to dusts 7-55
7-24 Summary of baseline human exposures to lead 7-56
7-25 Summary of potential additive exposures to lead 7-59
8-1 Estimated natural levels of lead in ecosystem 8-11
8-2 Estimates of the degree of contamination of herbivores,
omnivores, and carnivores 8-25
TCPBA/G
x
7/1/83
-------
2.
3.
J?
H
INTRODUCTION *'
CHEMICAL AND PHYSICAL PROPERTIES 3-1
3.1 INTRODUCTION 3-1
3.2 ELEMENTAL LEAD 3-1
3.3 GENERAL CHEMISTRY OF LEAD 3-2
3.4 ORGANOMETALLIC CHEMISTRY OF LEAD 3-3
3.5 FORMATION OF CHELATES AND OTHER COMPLEXES 3-4
3.6 REFERENCES 3-8
SAMPLING AND ANALYTICAL METHODS FOR ENVIRONMENTAL LEAO 4-1
4.1 INTRODUCTION 4-1
4.2 SAMPLING 4-2
A.g.l Regulatory Siting Criteria for Ambient Aerosol Samplers 4-2
I igjlitnt Sampling for Particulate and Gaseous Lead 4-6
i
¦ - -:c"" '' J III
-------
*1
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
slg
SLAMS
SMR
Sr
SRBC
SRMs
STEL
SW voltage
T-cells
t-tests
TBL
TEA
TEL
TIBC
TML
TMLC
TSH
TSP
U.K.
UHP
USPHS
VA
vIr
WHO
XRF
X*
Zn
ZPP
Surface immunoglobulin
State and local air monitoring stations
Standardized mortality ratio
Stronti um
Sheep red blood cells
Standard reference materials
Short-term exposure limit
Slow-wave voltage
Thymus-derived lymphocytes
Tests of significance
Tri-n-butyl lead
Tetraethyl-ammonium
Tetraethyllead
Total iron binding capacity
Tetramethyllead
Tetramethyl1ead chloride
Thyroid-stimulating hormone
Total suspended particulate
United Kingdom
Uridine monophosphate
U.S. Public Health Service
Veterans Administration
Deposition velocity
Visual evoked response
World Health Organization
X-Ray fluorescence
Chi squared
Zinc
Erythrocyte zinc protoporphyrin
MEASUREMENT ABBREVIATIONS
dl deciliter
ft feet
g gram
g/gal gram/gallon
g/ha*mo gram/hectare~month
km/hr ki1ometer/hour
1/min Uter/minute
mg/krn mi 11i gram/ki1ometer
Hg/m3 microgram/cubic meter
mm millimeter
jimol micrometer
ng/cm2 nanograms/square centimeter
nm namometer
nM nanomole
sec second
TCPBA/D
xiv
7/13/83
-------
PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
Page
7.3.1.1 Lead in Inhaled Air 7-39
7.3.1.2 Lead in Food 7-39
7.3.1.3 Lead in Drinking Water 7-47
7.3.1.4 Lead in Ousts . 7-50
7.3.1.5 Summary of Baseline Human Exposure to Lead 7-55
7.3.2 Additive Exposure Factors 7-56
7.3.2.1 Special Living and Working Environments 7-56
7.3.2.2 Additive Exposures Due to Age, Sex, or Socioeconomic
Status 7-65
7.3.2.3 Special Habits or Activities 7-65
7.3.3 Summary of Additive Exposure Factors 7-67
7.4 SUMMARY 7-67
8. EFFECTS OF LEAD ON ECOSYSTEMS 8-1
8.1 INTRODUCTION 8-1
8.1.1 Scope of Chapter 8 8-1
8.1.2 Ecosystem Functions 8-4
8.1.2.1 Types of Ecosystems 8-4
8.1.2.2 Energy Flow and Biogeochenical Cycles 8-4
8.1.2.3 Biogeochemistry of Lead 8-7
8.1.3 Criteria for Evaluating Ecosystem Effects 8-8
8.2 LEAD IN SOILS AND SEDIMENTS 8-12
8.2.1 Distribution of Lead in Soils 8-12
8.2.2 Origin and Availability of Lead in Aquatic Sediments 8-13
8.3 EFFECTS OF LEAD ON PUNTS 8-14
8.3.1 Effects on Vascular Plants and Algae 8-14
8.3.1.1 Uptake by Plants 8-14
8.3.1.2 Physiological Effects on Plants 8-17
8.3.1.3 Lead Tolerance in Vascular Plants 8-20
8.3.1.4 Effects of Lead on Forage Crops 8-21
8.3.1.5 Summary of Plant Effects 8-21
8.3.2 Effects on Bacteria and Fungi 8-21
8.3.2.1 Effects on Decomposers 8-21
8.3.2.2 Effects on Nitrifying Bacteria 8-24
8.3.2.3 Methylation by Aquatic Microorganisms 8-24
8.3.2.4 Sumary of Effects on Microorganisms 8-24
8.4 EFFECTS OF LEAD ON DOMESTIC AND WILD ANIMALS 8-25
8.4.1 Vertebrates 8-25
8.4.1.1 Terrestrial Vertebrates 8-25
8.4.1.2 Effects on Aquatic Vertebrates 8-27
8.4.2 Invertebrates : 8-30
8.4.3 Summary of Effects on Animals 8-33
8.5 EFFECTS OF LEAD ON ECOSYSTEMS 8-33
8.5.1 Delayed Decomposition 8-34
8.5.2 Circumvention of Calcium Biopurification 8-35
8.5.3 Population Shifts Toward Lead Tolerant Populations 8-37
8.5.4 Mass Balance Distribution of Lead in Ecosystems 8-37
8.6 SUMMARY 8-39
8.7 REFERENCES 8-41
TCP8A/E vii 7/1/83
-------
Chapter 4: Sampling and Analytical Methods for Environmental Lead
Principal Authors
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Contributing Author
Or. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80521
Dr. Robert Bruce
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. John B. Clements
Environmental Monitoring Systems Laboratory
MD-78
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. Tom Dzubay
Inorganic Pollutant Analysis Branch
MO-47
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. Samuel Lestz
Department of Mechanical
Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H. Liu
Department of Mechanical
Engineering
University of Minnesota
Minneapolis, MN 55455
Dr. Michael Oppenheimer
Environmental Oefense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. Bill Hunt
Monitoring and Data Analysis Division
MD-14
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Glen Sanderson
University of 111inois
Illinois Natural History Survey
Urbana, IL 61801
xv i
-------
PRELIMINARY DRAFT
LIST OF FIGURES (continued).
Figure Page
8-2 The ecological success of a population depends in part on the
availability of all nutrients at some optimum concentration 8-10
8-3 This figure attempts to reconstruct the right portion of a
tolerance curve 8-11
8-4 Within the decomposer food chain, detritus is progressively
broken down in a sequence of steps 8-23
8-5 The atomic ratios Sr/Ca, Ba/Ca and Pb/Ca (0) normally
decrease by several 8-36
TCP8A/F 7/1/83
-------
Dr. Ben Y. H, Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Or. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Uale University, School of Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr, James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
Or, Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Chapter 6: Transport and Transformation
Principal Author
Dr. Ron Bradow
Mobile Source Emissions Research Branch
M0-46
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Contributing Authors
Dr. Robert Elias Dr. Rodney Skogerboe
Environmental Criteria and Assessment Office Department of Chemistry
MD-52 Colorado State University
U.S. Environmental Protection Agency Fort Collins, CO 80521
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-M1le Road
Ferndale, MI 48220
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, Ml 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Or. Glen Sanderson
Illinois Natural History Survey
University of Illinois
Urbana, IL 61801
xviii
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS
AAS
Ach
ACTH
ADCC
ADP/O ratio
AIDS
AIHA
All
ALA
ALA-D
ALA-S
ALA-U
APOC
APHA
ASTM
ASV
ATP
B-cells
Ba
BAL
BAP
BSA
BUN
BW
C.V,
CaBP
CaEDTA
CBD
Cd
CDC
CEC
CEH
CFR
CMP
CNS
CO
COHb
CP-U
cBah
D.F.
DA
OCMU
DDP
DNA
DTH
EEC
EEG
EMC
EP
EPA
Atonic absorption spectrometry
Acetylcholine
Adrenocotlcotrophlc hormone
Antibody-dependent cell-mediated cytotoxicity
Adenosine diphosphate/oxygen ratio
Acquired immune deficiency syndrome
American Industrial Hygiene Association
Angiotensin II
Aminolevulinic acid
Aminolevulinic acid dehydrase
Aminolevulinic acid synthetase
Aminolevulinic acid in urine
Ammom um pyrrolidine-dithiocarbamate
American Public Health Association
Amercian Society for Testing and Materials
Anodic stripping voltaimetry
Adenosine triphosphate
Bone marrow-derived lymphocytes
Barium
British anti-Lewisite (AKA dimercaprol)
benzo(a)pyrene
Bovine serum albumin
Blood urea nitrogen
Body weight
Coefficient of variation
Calcium binding protein
Calcium ethylenediaminetetraacetate
Central business district
Cadmium
Centers for Disease Control
Cation exchange capacity
Center for Environmental Health
reference method
Cytidine monophosphate
Central nervous system
Carbon monoxide
Carboxyhemoglobin
Urinary coproporphyrin
plasma clearance of p-anrfnohippuric acid
Copper
Degrees of freedom
Dopamine
[3-(3,4-dichlorophenyl)-l,l~dii»ethylurea
Differential pulse polarography
Deoxyribonucleic acid
Delayed-type hypersensitivity
European Economic Community
Electroencephalogram
Encephal oatyocardi ti s
Erythrocyte protoporphyrin
U.S. Environmental Protection Agency
TCPBA/D
xi
7/13/83
-------
Dr. Irv Billick
Gas Research Institute
8600 West Sryn Mawr Avenue
Chicago, II 60631
Dr. Joe Boone
Clinical Chemistry and
Toxicology Section
Centers for Disease Control
Atlanta, GA 30333
Or. Robert Bornschein
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
Dr. Jack Dean
Imminobiology Program and
Iimunotoxicology/Cell Biology program
CUT
P.O. Box 12137
Research Triangle Park, NC 27709
Or. Fred deSerres
Associate Director for Genetics
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Robert Dixon
Laboratory of Reproductive and
Developmental Toxicology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Claire Ernhart
Department of Psychiatry
Cleveland Metropolitan General Hospital
Cleveland, OH 44109
Dr. Sergio Fachetti
Section Head - Isotope Analysis
Chemistry Division
Joint Research Center
121020 Ispra
Varese, Italy
Dr. Virgil Ferm
Department of Anatomy and Cytology
Dartmouth Medical School
Hanover, NH 03755
Mr. Jerry Cole
International Lead-Zinc Research
Organization
292 Madison Avenue
New York, NY 10017
Dr. Max Costa
Department of Pharmacology
University of Texas Medical
School
Houston, TX 77025
Dr. Anita Curran
Commissioner of Health
Westchester County
White Plains, NY 10607
Dr. Warren Galke
Department of Biostatisties
and Epidemiology
School of Allied Health
East Carolina University
Greenville, NC 27834
Mr. Eric Goldstein
Natural Resources Defense
Council, Inc.
122 E. 42nd Street
New York, NY 10168
Dr. Harvey Gonick
1033 Gayley Avenue
Suite 116
Los Angeles, CA 90024
Or. Robert Goyer
Deputy Director
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Stanley Gross
Hazard Evaluation Division
Toxicology Branch
U.S. Environmental Protection
Agency
Washi ngton, DC 20460
Dr. Paul Hammond
University of Cincinnati
Kettering Laboratory
Ci nci nnatl, OH 45267
xx
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued)
NA Not Applicable
NAAQS National ambient air quality standards
NADB National Aerometric Oata Bank
NAMS National Air Monitoring Station
NAS National Academy of Sciences
NASN National Air Surveillance Network
NBS National Bureau of Standards
NE Norepinephrine
NFAN National Filter Analysis Network
NFR-82 Nutrition Foundation Report of 1982
NHANES II National Health Assessment and Nutritional Evaluation Survey II
Ni Nickel
OSHA Occupational Safety and Health Administration
P Potassium
p Significance symbol
PAH Para-aminohippuric acid
Pb Lead
PBA Air lead
Pb(Ac)2 Lead acetate
PbB concentration of lead in blood
PbBrCl Lead (II) bromochloride
PBG Porphobilinogen
PFC Plaque-forming cells
pH Measure of acidity
PHA Phytohemagglutinin
PHZ Polyacrylamide-hydrous-zirconia
PIXE Proton-induced K-ray emissions
PMN Polymorphonuclear leukocytes
PND Post-natal day
PNS Peripheral nervous system
ppfli Parts per million
PRA Plasma renin activity
PRS Plasma renin substrate
PWM Pokeweed mitogen
Py-5-N Pyrimide-5'-nucleotidase
RBC Red blood cell; erythrocyte
RBF Renal blood flow
RCR Respiratory control ratios/rates
redox Oxidation-reduction potential
RES Reticuloendothelial system
RLV Rauscher leukemia virus
RNA Ribonucleic acid
S-HT Serotoni n
SA-7 Simian adenovirus
sen Standard cubic meter
S.D, Standard deviation
SOS Sodium dodecyl sulfate
S.E.M. Standard error of the mean
SES Socioeconomic status
SGOT Serum glutamic oxaloacetic transaminase
TCPBA/D x111 7/13/83
-------
Dr. Kathryn Mahaffey
Division of Nutrition
Food and Drug Administration
1090 Tusculum Avenue
Cincinnati, OH 45226
Dr. Ed McCabe
Department of Pediatrics
University of Wisconsin
Madison, WI 53706
Dr. Robert Putnam
International Lead-Zinc
Research Organization
292 Madison Avenue
New York, NY 10017
Dr. Michael Rabinowitz
Children's Hospital Medical
Center
300 Longwood Avenue
Boston, MA 02115
Dr. Paul Mushak
Department of Pathology
UNC School of Medicine
Chapel Hill, NC 27514
Or. John Rosen
Division of Pediatric Metabolism
Albert Einstein College of Medicine
Montefiore Hospital and Medical Center
111 East 210 Street
Bronx, NY 10467
Dr. Stephen R. Schroeder
Division for Disorders
of Development and Learning
Biological Sciences Research Center
University of North Carolina
Chapel Hill, NC 27514
Dr. Anna-Maria Seppalainen
Institutes of Occupational Health
Tyoterveyslaitos
Haartraaninkatu 1
00290 Helsinki 29
Finland
Dr. Harry Roels
Unite de Toxicologic
Industrielle et Medicale
Universite de Louvain
Brussels, Belgium
Dr. Ron Snee
E.I. duPont Nemours and
Company, Inc.
Engineering Department L3167
Wilmington, DE 19898
Mr. Gary Ter Haar
Toxicology and Industrial
Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Mr. Ian von Llndern
Department of Chemical
Engineering
University of Idaho
Moscow, ID 83843
Dr. Ellen Silbergeld
Environmental Defense Fund
1525 18th Street, NW
Washington, DC 20036
Dr. Richard P. Wedeen
V.A. Medical Center
Trenont Avenue
East Orange, NJ 07019
Chapter 8; Effects of Lead on Ecosystems
Principal Author
Dr. Robert Elias
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
xxii
-------
AUTHORS, CONTRIBUTORS, AND REVIEWERS
Chapter 3: Physical and Chemical Properties of Lead
Principal Author
Or. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Or. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y, H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Or. Michael Oppenheimer
Environnental Oefense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. William Pierson
Scientific Research
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Labs.
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Glen Sanderson
University of Illinois
Illinois Natural History Survey
Urbana, IL 61801
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
Baton Rouge, LA 70801
Or. Jams Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
XV
-------
-------
Mr*. Stan Sleva
Office of Air Quality Planning and Standards
MO-14
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of Forestry
New Haven, CT 06511
Or. Robert Stevens
Inorganic Pollutant Analysis Branch
MD-47
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Or. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Chapter 5: Sources and Emissions
Principal Author
Or. Janes Braddock
Mobile Source Emissions Research Branch
MD-46
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Contributing Author
Dr. Tom McMullen
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. William Plerson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Sien Sanderson
University of Illinois
Illinois Natural History Survey
Urbana, IL 61801
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
XV11
-------
PRELIMINARY DRAFT
via all routes and averaged over a suitable tine period, and the biological responses to those
levels be carefully assessed. Assessment of exposure must take into consideration the
temporal and spatial distribution of lead and its various forms in the environment.
This document focuses primarily on lead as found in its various forms in the ambient
atmosphere; in order to assess its effects on human health, however, the distribution and
biological availability of lead in other environmental media have been considered. The
rationale for structuring the document was based primarily on the two major questions of
exposure and response. The first portion of the document is devoted to lead in the environ-
ment—its physical and chemical properties; the monitoring of lead in various media;
sources, emissions, and concentrations of lead; and the transport and transformation of lead
within environmental media. The later chapters are devoted to discussion of biological
responses and effects on ecosystems and human health.
In order to facilitate printing, distribution, and review of the present draft materials,
this First External Review Draft of the revised EPA Air Quality Criteria Document for Lead
is being released in the form of four volumes. The first volume (Volume I) contains the
executive summary and conclusions chapter (Chapter 1) for the entire document. Volume II (the
present volume) contains Chapters 2-8, which include: the introduction for the document
(Chapter 2); discussions of the above listed topics concerning lead in the environment
(Chapters 3-7); and evaluation of lead effects on ecosystems (Chapter 8). The remaining two
volumes contain Chapters 9-13, which deal with the extensive available literature relevant to
assessment of health effects associated with lead exposure.
An effort has been made to limit the document to a highly critical assessment of the
scientific data base. The scientific literature has been reviewed through June 1983. The
references cited do not constitute an exhaustive bibliography of all available lead-related
literature but they are thought to be sufficient to reflect the current state of knowledge on
those issues most relevant to the review of the air quality standard for lead.
The status of control technology for lead is not discussed in this document. For infor-
mation on the subject, the reader Is referred to appropriate control technology documentation
published by the Office of Air Quality Planning and Standards (OAQPS), EPA. The subject of
adequate margin of safety stipulated in Section 108 of the Clean Air Act also Is not explicity
addressed here; this topic will be considered in depth by EPA's Office of Air Quality Planning
and Standards 1n documentation prepared as a part of the process of revising the National
Ambient Air Quality Standard for Lead.
D23PB2
2-2
7/1/83
-------
Or. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Dr. Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
Mew York, NY 10016
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Or. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
Chapter 7: Environmental Concentrations and Potential Pathways to Human
Exposure
Principal Authors
Dr. Cliff Davidson Dr. Robert Ellas
Department of Civil Engineering Environmental Criteria and
Carnegie-Mellon University Assessment Office
Schenley Park MD-52
Pittsburgh, PA 15213 U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. Carol Angle
Department of Pediatrics
University of Nebraska
College of Medicine
Omaha, NE 68105
Dr. Lee Annest
Division of Health Examin. Statistics
National Center for Health Statistics
3700 East-West Highway
Hyattsville, ND 20782
Or. Donald Barltrop
Department of Child Health
Westminister Children's Hospital
London SW1P 2NS
England
Dr. A. C. Chamberlain
Environmental and Medical
Sciences Division
Atomic Energy Research
Establishment
Harwell 0X11
England
Dr. Neil Chernoff
Division of Developmental Biology
MD-67
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Julian Chisolm
Baltimore City Hospital
4940 Eastern Avenue
Baltimore, MD 21224
xix
-------
PRELIMINARY DRAFT
TABLE 3-1. PROPERTIES OF ELEMENTAL LEAD
Property Description
Atomic weight 207.19
Atomic number 82
Oxidation states +2, +4
Density 11.35 g/cm3 at 20 °C
Melting point 327.5 °C
Boiling point 1740 °C
Covalent radius (tetradehral) 1.44 A
Ionic radii 1.21 A (+2), 0.78 I
Resistivity 21.9 x 10"6 ohm/cm
Natural lead is a mixture of four stable isotopes: 204Pb (*1.5 percent), 206Pb (23.6
percent), 207Pb (22.6 percent), and 208Pb (52.3 percent). There is no radioactive progenitor
for 204Pb, but 206Pb, 207Pb, and 208Pb are produced by the radioactive decay of 23
-------
Of. Alf Fischbein
Environmental Sciences Laboratory
Mt. Sinai School of Medicine
New York, NY 10029
Dr. Jack Fowle
Reproductive Effects Assessment Group
U.S. Environmental Protection Agency
RD-689
Washington, DC 20460
Dr. Bruce Fowler
Laboratory of Pharmacology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Or. Kristal Kostial
Institute for Medical Research
and Occupational Health
Yu-4100 Zagreb
Yugoslavia
Dr. Lawrence Kupper
Department of Biostatisties
UNO School of Public Health
Chapel Hill, NC 27514
Dr. Phillip Landrigan
Division of Surveillance,
Hazard Evaluation and Field Studies
Taft Laboratories - NIOSH
Cincinnati, OH 45226
Dr. David Lawrence
Microbiology and Immunology Dept.
Albany Medical College of Union
University
Albany, NY 1220*
Dr. Jane Lin-Fu
Office of Maternal and Child Health
Department of Health and Human Services
Rockville, MO 20857
Dr. Don lynam
Air Conservation
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. Ronald D. Hood
Department of Biology
The University of Alabama
University, AL 35486
Dr. V. Houk
Centers for Disease Control
1600 Clifton Road, NE
Atlanta, GA 30333
Dr. Loren 0. Koller
School of Veterinary Medicine
University of Idaho
Moscow, ID 83843
Dr. Chuck Nauman
Exposure Assessment Group
U.S. Environmental Protection
Agency
Washington, DC 20460
Dr. Herbert L. Needleman
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Dr. H. Mitchell Perry
V.A. Medical Center
St. Louis, MO 63131
Dr. Jack Pierrard
E.I. duPont de Nemours and
Compancy, Inc.
Petroleum Laboratory
Wilmington, DE 19898
Dr. Sergio Piomelli
Columbia University Medical School
Division of Pediatric Hematology
and Oncology
New York, NY 10032
Dr. Magnus Piscator
Department of Environmental Hygiene
The Karollnska Institute 104 01
Stockholm
Sweden
xxi
-------
PRELIMINARY DRAFT
The methyl compound, TML, is also manufactured by a Grignard process Involving the
electrolysis of lead pellets in methylmagnesium chloride (Shapiro and Frey, 1968):
2CH3MgCl + 2CH3C1 + Pb -~ (CH3)4Pb + 2MgCl2 (3-2)
A common type of commercial antiknock mixture contains a chemically redistributed mixture
of alkyllead compounds. In the presence of Lewis acid catalysts, a mixture of TEL and TML
undergoes a redistribution reaction to produce an equilibrium mixture of the five possible
tetraalkyllead compounds. For example, an equlmolar mixture of TEL and TML produces a product
with a composition as shown below:
Component MoT percent
(CH3)4Pb 4.6
(CH3)3Pb(C2H5) 24.8
(CH3)2Pb(C2Hs)2 41.2
(CH3)Pb(C2Hs)3 24.8
(C2H5)4Pb 4.6
These lead compounds are removed from internal combustion engines by a process called
lead scavenging, in which they react in the combustion chamber with halogenated hydrocarbon
additives (notably ethylene dibromide and ethylene dichloride) to form lead halides, usually
bromochlorolead(II). Mobile source emissions are discussed in detail in Section 5.3.3.2.
Several hundred other organolead compounds have been synthesized, and the properties of
many of them are reported by Shapiro and Frey (1968). The continuing Importance of organolead
chemistry is demonstrated by a variety of recent publications investigating the syntheses
(Hager and Huber, 1980, Wharf et al., 1980) and structures (Barkigla, et al., 1980) of
organolead complexes, and by recent patents for lead catalysts (Nishlkido, et al., 1980).
3.5 FORMATION OF CHELATES ANO OTHER COMPLEXES
The bonding in organometalUc derivatives of lead 1s principally covalent rather than
Ionic because of the small difference in the electronegativities of lead (1.8) and carbon
(2.6). As is the case in virtually all metal complexes, however, the bonding is of the
donor-acceptor type, in which both electrons in the bonding orbital originate from the carbon
atom.
The donor atoms in a metal complex could be almost any basic atom or molecule; the only
requirement 1s that a donor, usually called a ligand, must have a pair of electrons available
023PB3/A
3-4
7/13/83
-------
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Or. Derek Hodgson
Department of Chemsitry
University of North Carolina
Chapel Hill, NC 27514
Dr. David E. Koeppe
Department of Plant and Soil Science
P.O. Box 4169
Texas Technical University
Lubbock, TX 79409
Dr. Samuel lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H, Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Dr. Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Or. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr, Glen Sanderson
Illinois Natural History Survey
University of Illinois
Urbana, IL 61801
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
xxiii
-------
PRELIMINARY DRAFT
023PB3/A
H3C CH3
V
H3<^ CH3
H20
•
I
I
nh2
ch2
(a)
*
I
1
I
H2O
(b)
vbH2
9.0
4.5
s? 4 0
$
O 3.5
Z
£ 3.0
3
| 2.6
u
ec
O 2.0
a
Figure 3-1. Metal complexes of lead.
i—1—1—1—1—1—1—rVT
}
• Afl-
In-
—#Cu*
Hg
Pd*
••Pf
• Bl«*
>TI"
PMIV)
CLASS B _
• Pb"
Sn"» ecu-
cd'-e
N'VC°"
^ • •Nl"
In"
"*4
TVe^Zn*
• SWIM)
A*(lll)
• F»"
a»*e
SnIIV) ¦
BORDERLINE
i>. Lu"
CLASS A
4 6 8 10 12 14 16 20
CLASS A OR IONIC INDEX, Z*/r
Figure 3-2. Softness parameters of metals.
Source: Nieboer and Richardson (1980).
3-6
7/01/83
-------
PRELIMINARY DRAFT
2. INTRODUCTION
According to Section 108 of the Clean Air Act of 1970, as amended in June 1974, a cri-
teria document for a specific pollutant or class of pollutants shall
, . . accurately reflect the latest scientific knowledge useful in
indicating the kind and extent of all identifiable effects on public
health or welfare which may be expected from the presence of such pollu-
tant in the ambient air, in varying quantities.
Air quality criteria are of necessity based on presently available scientific data, which
in turn reflect the sophistication of the technology used in obtaining those data as well as
the magnitude of the experimental efforts expended. Thus air quality criteria for atmospheric
pollutants are a scientific expression of current knowledge and uncertainties. Specifically,
air quality criteria are expressions of the scientific knowledge of the relationships between
various concentrations—averaged over a suitable time period—of pollutants in the same atmos-
phere and their adverse effects upon public health and the environment. Criteria are issued
to help make decisions about the need for control of a pollutant and about the development of
air quality standards governing the pollutant. Air quality criteria are descriptive; that
1s, they describe the effects that have been observed to occur as a result of external expo-
sure at specific levels of a pollutant, in contrast, air quality standards are prescriptive;
that 1s, they prescribe what a political jurisdiction has determined to be the maximum per-
missible exposure for a given time in a specified geographic area.
In the case of criteria for pollutants that appear in the atmosphere only in the gas
phase (and thus remain airborne), the sources, levels, and effects of exposure must be con-
sidered only as they affect the human population through inhalation of or external contact
with that pollutant. Lead, however, is found In the atmosphere primarily as inorganic partic-
ulate, with only a small fraction normally occurring as vapor-phase organic lead. Conse-
quently, inhalation and contact are but two of the routes by which human populations may be
exposed to lead. Some particulate lead may remain suspended in the air and enter the human
body only by inhalation, but other lead-containing particles will be deposited on vegetation,
surface waters, dust, soil, pavements, interior and exterior surfaces of housing—in fact, on
any surface in contact with the air. Thus criteria for lead must be developed that will take
into account all principal routes of exposure of the human population.
This criteria document is a revision of the previous Air Quality Criteria Document for
Lead (EPA-600/8-77-017) published in December, 1977. This revision is mandated by the Clean
Air Act (Sect. 108 and 109), as amended U.S.C. §§7408 and 7409. The criteria document sets
forth what is known about the effects of lead contamination in the environment on human
health and welfare. This requires that the relationship between levels of exposure to lead,
D23PB2
2-1
7/1/83
-------
PRELIMINARY -ftftAFT
3.6 REFERENCES
Ahrland, S. (1966) Factors contributing to (b)-behaviour in acceptors. Struct. Bonding 1: 207-
220.
Ahrland, S. (1968) Thermodynamics of complex formation between hard and soft acceptors and
donors. Struct. Bonding (Berlin) 5: 118-149.
Ahrland, S. (1973) Thermodynamics of the stepwise formation of metal-ion complexes in aqueous
solution. Struct. Bonding (Berlin) 15; 167-188.
Barkigia, K. M.; Fajer, J.; Adler, A. D.; Williams, 6. J. 8. (1980) Crystal and molecular struc-
ture of (5,10,15,20-tetra-n-propylporphinato)lead(II): a "roof" porphyrin. Inorg. Chen.
19: 2057-2061.
Basolo, F.; Pearson, R. G. (1967) Mechanisms of inorganic reactions: a study of metal complexes
in solution. New York, NY: John Wiley & Sons, Inc.; pp. 23-25, 113-119.
Britton, D. (1964) The structure of the Pbg 4 ion. Inorg. Chem. 3: 305.
Carty, A. J.; Taylor, N. J. (1976) Binding of inorganic mercury at biological sites. J. Chem.
Soc. Chem. Commun. (6): 214-216.
Carty, A. J.; Taylor, N. J. (1977) Binding of heavy metals at biologically important sites:
synthesis and molecular structure of aquo(bromo)-DL-pen1c11laminatocadnrium(II) d1hydrate.
Inorg. Chem. 16: 177-181.
Cotton, F. A.; Wilkinson, G. (1980) Advanced inorganic chemistry. New York, NY: John Wiley &
Sons, Inc.
de Meester, P.; Hodgson, 0. J. (1977a) Model for the binding of D-pen1c111amine to metal ions
in living systems: synthesis and structure of l-histidinyl-D-penicillaminatocobalt(III)
monohydrate, [Co(L-his)(D-pen)] Hz0. J. Am. Chem. Soc. 99: 101-104.
de Meester, P.; Hodgson, D. J. (1977b) Synthesis and structural characterization of l-
hi sti di nato-0-penic i11 aminatochromi urn (III) monohydrate. J. Chem. Soc. Dal ton Trans. (17):
1604-1607.
de Meester, P.; Hodgson, D, J. (1977c) Absence of metal interaction with sulfur in two metal
complexes of a cysteine derivative: the structural characterization of Bis(S-methyl-L-
cysteinato)cactaium(11) and B1s(S-methyl-L-cysteinato)zinc(II). J. Am. Chem. Soc. 99: 6884-
6889*
Ooe, B. R. (1970) Lead isotopes. New York, NY: Springer-Verlag. (Engelhardt, W.; Hahn, T.; Roy,
R.; Winchester, J. W.; Wyllie, P. J., eds. Minerals, rocks and inorganic materials:
monograph series of theoretical and experimental studies: v. 3).
Dyrssen, D. (1972) The changing chemistry of the oceans. Ambio 1: 21*25.
Freeman, H. C.; Stevens, G. N.; Taylor, I. F., Jr. (1974) Metal binding in chelation therapy:
the crystal structure of D-penicillaminatolead(II). J. Chem. Soc. Chem. Commun. (10):
366-367.
Freeman, H. C.; Huq, F.; Stevens, G. N. (1976) Metal binding by D-penlcillamine: crystal struc-
ture of D-penicl11 aminatocadmium(II) hydrate. J. Chem. Soc. Chem. Commun. (3): 90-91.
A03REF/A 3-8 7/13/83
-------
PRELIMINARY DRAFT
3. CHEMICAL AND PHYSICAL PROPERTIES
3,1 INTRODUCTION
Lead is a gray-white metal of bright luster that, because of its easy isolation and low
melting point (327.5°C), was among the first of the metals to be placed in the service of man.
Lead was used as early as 2000 B.C. by the Phoenicians, who traveled as far as Spain and
England to mine it, and it was used extensively by the Egyptians; the British Museum contains
a lead figure found in an Egyptian temple which possibly dates from 3000 B.C. The most
abundant ore is galena, In which lead is present as the sulfide (PbS), and from which metallic
lead is readily smelted. The metal is soft, malleable, and ductile, a poor electrical
conductor, and highly impervious to corrosion. This unique combination of physical properties
has led to its use in piping and roofing, and in containers for corrosive liquids. By the
time of the Roman Empire, it was already in wide use in aqueducts and public water systems, as
well as in cooking and storage utensils. Its alloys are used as solder, type metal, and
various antifriction materials. The metal and the dioxide are used in storage batteries, and
much metal is used in cable covering, plumbing and ammunition. Because of Its high nuclear
cross section, lead is extensively used .as a radiation shield around X-ray equipment and
nuclear reactors.
3.2 ELEMENTAL LEAD
In comparison with the most abundant metals in the earth's crust (aluminum and iron),
lead is a rare metal; even copper and zinc are more abundant by factors of five and eight,
respectively. Lead is, however, more abundant than the other toxic heavy metals; its
abundance in the earth's crust has been estimated (Moeller, 1952) to be as high as 1.6 x 10 3
percent, although some other authors (Heslop and Jones, 1976) suggest a lower value of 2 x
10 4 percent. Either of these estimates suggests that the abundance of lead is more than 100
times that of cadmium or mercury, two other significant systemic metallic poisons. More
important, since lead occurs in highly concentrated ores from which it is readily separated,
the availability of lead is far greater than its natural abundance would suggest. The great
environmental significance of lead is the result both of its utility and of Its availability.
Lead ranks fifth among metals in tonnage consumed, after iron, copper, aluminum and zinc; it
is, therefore, produced in far larger quantities than any other toxic heavy metal (Dyrssen,
1972). The properties of elemental lead are summarized in Table 3-1.
023PB3/A
3-1
7/13/83
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PRELIMINARY DRAFT
Shaw, C. F., III; Allred, A. L. (1970) Nonbonded Interactions 1n organometallic compounds of
Group IV B. Organometallic Chem. Rev. A 5: 95-142.
Wharf, I.; Onyszchuk, M.; Miller, J. M.; Jones, T. R. B. (1980) Synthesis and spectroscopic
studies of phenyl lead halide and thiocyanate adducts with hexamethy1phosphorami de. J.
Organomet. Chem. 190; 417-433.
Williams, M. W.; Hoeschele, J. D.; Turner, J. E.; Jacobson, K. B.; Christie, N. T.; Paton,
C. L.; Smith, L. H.; Witsch, H. R.; Lee, E. H. (1982) Chemical softness and acute metal
toxicity in mice and Drosoohila. Toxicol. Appl. Pharmacol. 63: 461-469.
Williams, M. W.; Turner, J. E. (1981) Comments on softness parameters and metal ion toxicity.
J. Inorg. Nucl. Chem. 43; 1689-1691.
Wong, Y. S.; Chieh, P. C.; Carty, A. J. (1973) Binding of methyl mercury by ami no-acids: X-ray
structures of DJL-peni c il 1 ami natonethy 1 mercury( 11). J. Chem. Soc. Chem. Comtiun. (19):
741-742.
03REF
3-10
7/1/83
-------
PRELIMINARY DRAFT
the tetravalent (+4) oxidation state. This Important chemical feature 1s a direct result of
the fact that the strengths of single bonds between the Group IV atoms and other atoms
generally decrease as the atomic number of the Group IV atom Increases (Cotton and Wilkinson,
1980). Thus, the average energy of a C-H bond Is 100 kcal/mole, and 1t Is this factor that
stabilizes CH« relative to CH2; for lead, the Pb-H energy is only approximately 50 kcal/mole
(Shaw and Allred, 1970), and this Is presumably too small to compensate for the Pb(II) +
Pb(IV) promotional energy. It Is this same feature that explains the marked difference in the
tendencies to catenation shown by these elements. Though C-C bonds are present in literally
millions of compounds, for lead catenation occurs only in organolead compounds, lead does,
however, form compounds like Na4Pb9 which contain distinct polyatomic lead clusters (Brltton,
1964), and Pb-Pb bonds are found in the cationic cluster [Pbs0(0H)e]+4 (011n and Soderquist,
1972).
A listing of the solubilities and physical properties of the more common compounds of
lead is given 1n Appendix 3A. As can be discerned from those data, most inorganic lead salts
are sparingly soluble (e.g., PbF2, PbCl2) or virtually insoluble (PbS04, PbCr04) in water; the
notable exceptions are lead nitrate, Pb(N03)2, and lead acetate, Pb(0C0CH3)2. Inorganic lead
(II) salts are, for the most part, relatively high-melting-point solids with correspondingly
low vapor pressures at room temperatures. The vapor pressures of the most commonly
encountered lead salts are also tabulated in Appendix 3A. The transformation of lead salts in
the atmosphere 1s discussed in Chapter 6.
3.4 0RGAN0METALLIC CHEMISTRY OF LEAD
The properties of organolead compounds (i.e., compounds containing bonds between lead and
carbon) are entirely different from those of the inorganic compounds of lead; although a few
organolead(II) compounds, such as dicyclopentadlenyllead, Pb(CsH5)2, are known, the organic
chemistry of lead is dominated by the tetravalent (+4) oxidation state. An Important property
of most organolead compounds is that they undergo photolysis when exposed to light (Rufman and
Rotenberg, 1980).
Because of their use as antiknock agents in gasoline and other fuels, the most important
organolead compounds have been the tetraalkyl compounds tetraethyllead (TEL) and
tetramethyllead (TML). As would be expected for such nonpolar compounds, TEL and TML are
insoluble in water but soluble in hydrocarbon solvents (e.g., gasoline). These two compounds
are manufactured by the reaction of the alky! chloride with lead-sodium alloy (Shapiro and
Frey, 1968);
4NaPb ~ 4C2H5C1 ~ (C2H6)4Pb ~ 3Pb + 4NaCl (3-1)
023PB3/A
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7/13/83
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PRELIMINARY DRAFT
Table 3A-1. (continued). PHYSICAL PROPERTIES OF INORGANIC LEAD COMPOUNDS1
Solubility, g/100 ml
Cold Hot Other
Compound
Formula
M.W.
S.G.
M.P.
water
water solvents
Nitrate, basic
Pb(0H)N03
286.20
5.93
dl80
19.4
s
sa
Oxalate
PbC204
295.21
5.28
d300
0.00016
sa
Oxide
PbO
223.19
9.53
888
0.0017
s,alk
Oioxide
Pb02
239.19
9.375
d290
i
1
sa
Oxide (red)
Pb304
685.57
9.1
d500
i
i
sa
Phosphate
Pba(P04)2
811.51
7
1014
1.4x10"6
1
s,alk
Sulfate
PbS04
303.25
6.2
1170
0.00425
0.0056
Sulfide
PbS
239.25
7.5
1114
8.6x10"5
sa
Sulfite
PbS03
287.25
d
1
1
sa
Thiocyanate
Pb(SCN)2
323.35
3.82
dl90
0.05
0.2
s,alk
Abbreviations: a - acid; al - alcohol; alk - alkali; d - decomposes;
expl - explodes; glyc - glycol; i - insoluble; s - soluble;
M.W. - molecular weight; S.G. - specific gravity; and
M.P. - aelting point.
Source: Weast, 1975.
PBAPP/A
3A-2
7/1/83
-------
PRELIMINARY DRAFT
for bond formation. In general, the metal atom occupies a central position in the complex, as
exemplified by the lead atom in tetramethyllead (figure 3-la) which is tetrahedrally
surrounded by four methyl groups. In these simple organolead compounds, the lead is usually
present as Pb(IV), and the complexes are relatively inert. These simple ligands, which bind
to metal at only a single site, are called monodentate ligands. Some ligands, however, can
bind to the metal atom by more than one donor atom, so as to form a heterocyclic ring
structure. Rings of this general type are called chelate rings, and the donor molecules which
form them are called polydentate ligands or chelating agents. In the chemistry of lead,
chelation normally involves Pb(ll), leading to kinetically quite labile (although
thermodynamically stable) octahedral complexes. A wide variety of biologically significant
chelates with ligands, such as amino acids, peptides, nucleotides and similar macromolecules,
are known. The simplest structure of this type occurs with the amino acid glycine, as
represented in Figure 3-lb for a 1:2 (metal:ligand) complex. The importance of chelating
agents in the present context is their widespread use in the treatment of lead and other metal
poisoning.
Metals are often classified according to some combination of their electronegativity,
ionic radius and formal charge (Ahrland, 1966, 1968, 1973; Basolo and Pearson, 1967; Nieboer
and Richardson, 1980; Pearson, 1963, 1968). These parameters are used to construct empirical
classification schemes of relative hardness or softness. In these schemes, "hard" metals form
strong bonds with "hard" anions and likewise "soft" metals with "soft" anions. Some metals
are borderline, having both soft and hard character. Pb(II), although borderline,
demonstrates primarily soft character (Figure 3-2). The terms Class A may also be used to
refer to hard metals, and Class B to soft metals. Since Pb(II) is a relatively soft (or class
B) metal ion, it forms strong bonds to soft donor atoms like the sulfur atoms in the cysteine
residues of proteins and enzymes; it also coordinates strongly with the imidazole groups of
histidine residues and with the carboxyl groups of glutamic and aspartic acid residues. In
living systems, therefore, lead atoms bind to these peptide residues in proteins, thereby
preventing the proteins from carrying out their functions by changing the tertiary structure
of the protein or by blocking the substrate's approach to the active site of the protein. As
has been demonstrated in several studies (Jones and Vaughn, 1978; Williams and Turner, 1981;
Williams et al., 1982), there is an inverse correlation between the LD50 values of metal
complexes and the chemical softness parameter (op) (Pearson and Mawby, 1967). Thus, for both
mice and Drosophila, soft metal ions like lead(TI) have been found to be more toxic than hard
metal ions (Williams et al., 1982). This classification of metal ions according to their
toxicity has been discussed in detail by Nieboer and Richardson (1980). Lead(II) has a higher
softness parameter than either cadmium(II) or mercury(II), so lead(II) compounds would not be
expected to be as toxic as their cadmium or mercury analogues.
023PB3/A 3-5 7/13/83
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PRELIMINARY DRAFT
For a given metal, M, arid two ligands, B and B-8, which are chemically similar, It 1s
established that and ka have similar values to each other, as do k2 and and and kd;
each of these pairs of terms represents chemically similar processes. The origin of the
chelate effect lies in the very large value of k3 relative to that of kc> This comes about
because kg represents a unimolecular process, whereas kc is a bimolecular rate constant.
Consequently , Kg » Ki.
This concept can, of course, be extended to polydentate ligands; in general, the more
extensive the chelation, the more stable the metal complex. Hence, one would anticipate,
correctly, that polydentate chelating agents such as penicillamine or EOTA can form extremely
stable complexes with metal 1ons.
3A.3 REFERENCES
StuH, D. R. (1947) Vapor pressure of pure substances: organic compounds. Ind. Eng. Chem 39:
517-540.
Weast, R.C., ed. (1975) Handbook of chemistry and physics. Cleveland, OH; The Chemical Rubber
Co.
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PRELIMINARY DRAFT
/
O
II
CH2-C-0-
/
N-CH2-CH2-N
\
-O-C-CH2
II
CH2-C-O-
o
£DTA
PENICILLAMINE
Figure 3-3. Structure of chelating agents.
The role of the chelating agents is to compete with the peptides for the Metal by forcing
stable chelate complexes that can be transported fro* the protein and eventually be exreted by
the body. For simple thermodynamic reasons (see Appendix 3A), chelate complexes are much more
stable than monodentate metal complexes, and it is this enhanced stability that is the basis
for their ability to compete favorably with proteins and other ligands for the metal ions.
The chelating agents most commonly used for the treatment of lead poisoning are ethylenediami-
netetraacetate ions (EDTA), 0-penici11amine (Figure 3-3) and their derivatives. EDTA is known
to act as a hexadentate ligand toward metals (Lis, 1978; McCandlish et al., 1978). X-ray
diffraction studies have demonstrated that D-penici11 amine is a tridentate ligand binding
through its sulfur, nitrogen and oxygen atoms to cobalt (de Meester and Hodgson, 1977a; Helis;
et al., 1977), chromium (de Meester and Hodgson, 1977b), cadmium (Freeman et al., 1976), and
lead itself (Freeman et al., 1974), but both penicillamine and other cysteine derivatives may
act as bidentate ligands (Carty and Taylor, 1977; de Heester and Hodgson, 1977c). Moreover,
penicillamine binds to mercury only through its sulfur atoms (Wong et al., 1973; Carty and
Taylor, 1976).
It should be noted that both the stoichiometry and structures of metal chelates depend
upon pH, and that structures different from those manifest in solution may occur in crystals.
It will suffice to state, however, that several ligands can be found that are capable of suffi-
ciently strong chelation with lead present in the body under physiological conditions to per-
mit their use in the effective treatment of lead poisoning.
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PRELIMINARY DRAFT
4.2 SAMPLING
The purpose of sampling is to determine the nature and concentration of lead in the envi-
ronment. Sampling strategy is dictated by research needs. This strategy encompasses site
selection, choice of instrument used to obtain representative samples, and choice of method
used to preserve sample integrity. In the United States, sampling stations for air pollutants
have been operated since the early 1950's. These early stations were a part of the National
Air Surveillance Network (NASN), which has now become the National Filter Analysis Network
(NFAN). Two other types of networks have been established to meet specific data requirements.
State and Local Air Monitoring Stations (SLAMS) provide data from specific areas where pollu-
tant concentrations and population densities are the greatest and where monitoring of compli-
ance to standards is critical. The National Air Monitoring Station (NAMS) network is designed
to serve national monitoring needs, including assessment of national ambient trends. SLAMS
and NAMS stations are maintained by state and local agencies and the air samples are analyzed
in their laboratories. Stations in the NFAN network are maintained by state and local agen-
cies, but the samples are analyzed by laboratories in the U.S. Environmental Protection
Agency, where quality control procedures are rigorously maintained.
Data from all three networks are combined into one data base, the National Aerometric
Data Bank (NADB). These data may be Individual chemical analyses of a 24-hour sampling period
arithmetically averaged over a calendar period, or chemical composites of several filters used
to determine a quarterly composite. Data are occasionally not available because they do not
conform to strict statistical requirements. A summary of the data from the NADB appears in
Section 7.2.1.
4.2.1 Regulatory Siting Criteria for Ambient Aerosol Samplers
In September of 1981, EPA promulgated regulations establishing ambient air monitoring and
data reporting requirements for lead [C.F.R. (1982) 40:§583 comparable to those already estab-
lished 1n May of 1979 for the other criteria pollutants. Whereas sampling for lead is accomp-
lished when sampling for TSP, the designs of lead and TSP monitoring stations must be comple-
mentary to insure compliance with the NAMS criteria for each pollutant, as presented in Table
4-1, Table 4-2, and Figure 4-1.
In general, the criteria with respect to monitoring stations designate that there must be
at least two SLAMS sites for lead 1n any area which has a population greater than 500,000 and/
or any area where lead concentration currently exceeds the ambient lead standard (1.5 jig/m3)
or has exceeded It since January 1, 1974. In such areas, the SLAMS sites designated as part
of the NAMS network must include a microscale or middlescale site located near a major roadway
(230,000 ADT), as well as a neighborhood scale site located in a highly populated residential
sector with high traffic density (230,000 ADT).
023PB4/A 4-2 7/14/83
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PRELIMINARY DRAFT
Freeman, H. C.; Huq, F.; Stevens, 6. N. (1976) Metal binding by D-penicmamine: crystal struc-
ture of D-penic1llam1natocadm1u*(II) hydrate. J. Chem. Soc. Chem. Commun. (3): 90-91.
Hager, C-D.; Huber, F. (1980) Organoblelverbindungen von MercaptocarbonsSuren. [Organolead com-
pounds of mercaptocarboxyl1c acids.] Z. Naturforsch. 35b: 542-547.
Hells, H. M.; de Meester, P. j Hodgson, D. J. (1977) Binding of penicillamine to toxic metal
Ions: synthesis and structure of potassium(D-penici11 aminato) (L-Penicillaminato)cobal-
tate(III) d1hydrate, K[Co(0-pen)(L-pen)] 2H20. J. Am. Chen. Soc. 99: 3309-3312.
Heslop, R. B.; Jones, K. (1976) Inorganic chemistry: a guide to advanced study. New York, NY:
Elsevier Science Publishing Co.; pp. 402-403.
Jones, M. M.; Vaughn, W. K. (1978) HSAB theory and acute metal ion toxicity and detoxification
processes. J. Inorg. Nucl. Chem. 40: 2081-2088.
Lis, T. (1978) Potassium ethylenedlanilnetetraacetatomanganate(III) dihydrate. Acta Crystallogr.
Sec. B 34: 1342-1344.
McCandlish, E. F. K.; Michael, T. K.; Neal, J. A.; Lingafelter, E. C.; Rose, N. J. (1978) Com-
parison of the structures and aqueous solutions of [o-phenylenedlaminetetraacetato(4-)]
cobalt(II) and [ethylenediaminetetraacetato(4-)] cobaTt(II) ions. Inorg. Chem. 17: 1383-
1394.
Moeller, T. (1952) Inorganic chemistry: an advanced textbook. New York, NY: John Wiley & Sons,
Inc.
Nieboer, E.; Richardson, D. H. S. (1980) The replacement of the nondescript term "heavy metals"
by a biologically and chemically significant classification of metal ions. Environ.
Pollut. Ser. B. 1: 3-26.
Nishikldo, J. j Tamura, N.; Fukuoka, Y. (1980) (Asahi Chemical Industry Co. Ltd.) Ser. Patent
No. 2,936,652.
OHn, A.; SBderqulst, R. (1972) The crystal structure of p-[Pb#0(OH)6](C104)4 Hz0. Acta Chem.
Scand. 26: 3505-3514.
Pearson, R. G. (1963) Hard and soft acids and bases. J. Am. Chem. Soc. 85: 3533-3539.
Pearson, R. G. (1968) Hard and soft acids and bases, HSAB, part 1: fundamental principles. J.
Chem. Educ. 45: 581-587.
Pearson, R. G.; Mawby, R. J. (1967) The nature of metal-halogen bonds. In: Gutmann, V., ed.
Halogen chemistry: vol. 3. New York, NY: Academic Press, Inc.; pp. 55-84.
Rufman, N. M.; Rotenberg, 2. A. (1980) Special kinetic features of the photodecomposltlon of
organolead compounds at lead electrode surfaces. Sov, Electrochem. Engl. Transl. 16:
309-314.
Russell, R.; Farquhar, R. (1960) Introduction. In: Lead isotopes in geology. New York, NY:
Interscience; pp. 1-12.
Shapiro, H.; Frey, F. W. (1968) The organic compounds of lead. New York, NY: John Wiley & Sons.
(Seyferth, D., ed. The chemistry of organometalllc compounds: a series of monographs.)
03REF
3-9
7/1/83
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PRELIMINARY DRAFT
TABLE 4-2. TSP NAMS CRITERIA
Approximate Number of Stations Per Area
Population Category
High1
Concentration
Medium2
Low3
High — >500,000
6-8
4-6
0-2
Medium -- 100-500,000
4-6
2-4
0-2
Low — 50-100,000
2-4
1-2
0
JWhen TSP Concentration exceeds by 20* Primary Ambient Air Standard of 75 MS/®3 annual
geometric mean.
2TSP Concentration > Secondary Ambient Air Standard of 60 Hfl/»3 annual geometric lean.
sTSP Concentration < Secondary Ambient Air Standard.
Source: C.F.R. (1982) 40:§58 App D
With respect to the siting of monitors for lead and other criteria pollutants, there are
standards for elevation of the monitors above ground level, setback fro* roadways, and setback
from obstacles. A summary of the specific siting requirements for lead Is presented in Table
4-1 and summarized below:
• Samples must be placed between 2 and 15 meters from the ground and greater than 20
meters from trees.
• Spacing of samplers from roads should vary with traffic volume; a range of 5 to
100 meters from the roadway is suggested.
• Distance from samplers to obstacles must be at least twice the height the obstacle
protrudes above the sampler.
• There must be a 270° arc of unrestricted air flow around the monitor to include
the prevailing wind direction that provides the maximum pollutant concentration to
the monitor.
• No furnaces or incineration flues should be in close proximity to the monitor.
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APPENDIX 3A
PHYSICAL/CHEMICAL DATA FOR LEAD COMPOUNDS
3A.1 DATA TABLES
Table 3A-1. PHYSICAL PROPERTIES OF INORGANIC LEAD COMPOUNDS1
Solubility. o/lOO ml
——¦—ii ii'i i
Compound
Foraula
M.W.
S.G.
M, P.
Cold
water
Hot
water
Other
solvents
Lead
Pb
207.19
11.35
327.5
i
1
sa
Acetate
Pb(C2Hg02)2
325.28
3.25
280
44.3
22150
s glyc
Azide
Pb(Ns)t
291.23
-
expl.
0.023
0.09"
-
Brornate
Pb(BrO3)2*H20
481.02
5.53
dl80
1.38
si s
-
Bromide
PbBr2
367.01
6.66
373
0.8441
4 71100
sa
Carbonate
PbC03
267.20
6.6
d315
0.00011
d
sa.alk
Carbonate,
basic
2PbC0s-Pb(0H)2
775,60
6.14
d400
i
1
s HN0S
Chloride
PbCl2
278.10
5.85
501
0.99
3.34100
i al
Chlorobromide
PbClBr
322.56
Chronate
PbCr04
323.18
6.12
844
6xl0"«
i
sa.alk
Chromate,
basic
PbCr04-Pb0
546.37
6.63
1
1
sa.alk
Cyanide
Pb(CN)2
259.23
si s
s
s KCN
Fluoride
PbF2
245.19
8.24
855
0.064
s HN0s
Fluorochloride
PbFCl
261.64
7.05
601
0.037
0.1081
Fornate
Pb(CH02)2
297.23
4.63
dl90
1.6
20
i al
Hydride
PbH2
209.21
d
Hydroxide
Pb(0H}2
241.20
dl45
0.0155
si s
sa.alk
Iodate
Pb{IOs)2
557.00
6.155 d300
0.0012
0,003
s HN0s
Iodide
Pbl2
461.00
6.16
402
0.063
0.41
s,alk
Nitrate
Pb(N03)2
331.20
4.53
d470
37.65
127
s.alk
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To clarify the relationship between monitoring objectives and the actual siting of a mon-
itor, the concept of a spatial scale of representativeness was developed. The spatial scales
are described in terms of the physical dimensions of the air space surrounding the monitor
throughout which pollutant concentrations are fairly similar. Table 4-3 describes the scales
of representativeness while Table 4-4 relates monitoring objectives to the appropriate spatial
scale.
The time scale may also be an important factor. A study by Lynam (1972) illustrates the
effect of setback distance on short-term (15 minute) measurements of lead concentrations
directly downwind from the source. They found sharp reductions in lead concentration with in-
creasing distance from the roadway. A similar study by PEDCo Environmental, Inc. (1981) did
not show the same pronounced reduction when the data were averaged over monthly or quarterly
time periods. The apparent reason for this effect is that windspeed and direction are not
consistent. Therefore, siting criteria must include sampling times sufficiently long to
include average windspeed and direction, or a sufficient number of samples must be collected
over short sampling periods to provide an average value consistent with a 24-hour exposure.
4.2.2 Ambient Sampling for Particulate and Gaseous lead
Airborne lead is primarily inorganic particulate matter but may occur in the form of
organic gases. Devices used for collecting samples of ambient atmospheric lead include the
standard hi-vol and a variety of other collectors employing filters, impactors, inpingers, or
scrubbers, either separately or in combination. Some samplers measure total particulate
matter gravlmetrically; thus the lead data are usually expressed in pg/g PM or pg/m3 air.
Other samplers do not measure PM gravimetrically; therefore, the lead data can only be
expressed as pg/m3. Some samplers measure lead deposition expressed in pg/cm2. Some instru-
ments separate particles by size. As a general rule, particles smaller than 2,5 pm are
defined as fine, and those larger than 2.5 pm are defined as coarse.
In a typical sampler, the ambient air is drawn down into the inlet and deposited on the
collection surface after one or more stages of particle size separation. Inlet effectiveness,
internal wall losses, and retention efficiency of the collection surface may bias the
collected sample by selectively excluding particles of certain sizes.
4.2.2.1 High Volume Sampler (hi-vol). The present SLAMS and NAMS employ the standard hi-vol
sampler (Robson and Foster, 1962; Silverman and Viles, 1948; U.S. Environmental Protection
Agency, 1971) as part of their sampling networks. As a Federal Reference Method Sampler, the
hi-vol operates with a specific flow rate range of 1.13 to 1.70 mVmin, drawing air through a
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PRELIMINARY DRAFT
Table 3A-2. TEMPERATURE VARIATION OF THE VAPOR PRESSURES
OF COMMON LEAO COMPOUNDS
Temperature °C
Name
Formula
M.P.
1 mm
10 mm
40 mm
100 mm
400 mm
760 mm
Lead
Pb
327.4
973
1162
1309
1421
1630
1744
Lead
bromide
PbBr2
373
513
610
686
745
856
914
Lead
chloride
PbCl 2
501
547
648
725
784
893
954
Lead
flouride
PbF2
855
sol id
904
1003
1080
1219
1293
Lead
iodide
Pbl2
402
479
571
644
701
807
872
Lead
oxide
PbO
890
943
1085
1189
1265
1402
1472
Lead
sulfide
PbS
1114
852
975
1048
1108
1221
1281
(solid)
(solid)
(solid)
(solid)
Source: Stull, 1947
3A.2. THE CHELATE EFFECT
The stability constants of chelated complexes are normally several orders of magnitude
higher than those of comparable monodentate complexes; this effect is called the chelate
effect, and is very readily explained in terms of kinetic considerations. A comparison of the
binding of a single bldentate ligand with that of two molecules of a chemically similar mono-
dentate ligand shows that, for the monodentate case, the process can be represented by the
equations:
M + B * M-B (3A-1)
M-B ~ B
b
kc MB2 (3A-2)
kd
The related expressions for the bidentate case are:
ki
M + B-B M-B-B (3A-3)
k2
k3 M B (3A-4)
M-B-B k4 B
The overall equilibrium constants, therefore, are:
ki - kakc. K2 _ k'ks
™~ i. L ) ^ t
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PRELIMINARY DRAFT
200 x 250 mm glass fiber filter. At these flow rates, 1600 to 2500 m3 of air per day are
sampled. Many hi-vol systems are presently equipped with mass flow sensors to control the
total flow rate through the filter.
The present hi-vol approach has been shown, during performance characterization tests, to
have a number of deficiencies. First, wind tunnel testing by Wedding et al. (1977) has shown
that the inlet characteristics of the hi-vol sampler are strongly affected by particle size,
windspeed, and wind direction. However, since most lead particles have been shown to have a
mass median diameter (MM0) in the range of 0.25 to 1.4 pm (Lee and Goranson, 1972), the hi-vol
sampler should present reasonably good estimates of ambient lead concentrations. However, for
particles greater than 5 m">. the hi-vol system is unlikely to collect representative samples
(McFarland and Rodes, 1979; Wedding et al., 1977). In addition, Lee and Wagman (1966) and
Stevens et al. (1978) have documented that the use of glass fiber filters leads to the forma-
tion of artifactual sulfate. Splcer et al. (1978) suggested a positive artifactual nitrate,
while Stevens et al. (1980) showed both a positive and negative artifact may occur with glass
or quartz filters when using a hi-vol sampler.
4.2.2.2 Oichotomous Sampler. The diehotomous sampler collects two particle size fractions,
typically 0 to 2.5 p" and 2.5 p® to the upper cutoff of the inlet employed (normally 10 pn).
The impetus for the dichoton^ of collection, which approximately separates the fine and coarse
particles, was provided by Whitby et al. (1972) to assist in the identification of particle
sources. A 2.5 pit cutpoint for the separator was also recommended by Miller et al. (1979) be-
cause it satisfied the requirements of health researchers interested in respirable particles,
provided adequate separation between two naturally occurring peaks in the size distribution,
and was mechanically practical. Because the fine and coarse fractions collected in most loca-
tions tend to be acidic and basic, respectively, this separation also minimizes potential par-
ticle interaction after collection.
The particle separation principle used by this sampler was described by Hounaa and
Sherwood (1965) and Conner (1966). The version now in use by EPA was developed by Loo et al.
(1979). The separation principle involves acceleration of the particles through a nozzle.
Ninety percent of the flowstream is diverted to a small particle collector, while the larger
particles continue by inertia toward the large particle collection surface. The inertia!
virtual lipactor design causes" 10 percent of the fine particles to be collected with the
coarse particle fraction. Therefore, the mass of fine and coarse particles must be adjusted
to allow for their cross contamination. This mass correction procedure has been described by
Dzubay et al. (1982).
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4. SAMPLING AND ANALYTICAL METHODS FOR ENVIRONMENTAL LEAD
4.1 INTRODUCTION
Lead, like all criteria pollutants, has a designated Reference Method for monitoring and
analysis as required in State Implementation Plans for determining compliance with the lead
National Ambient Air Quality Standard. The Reference Method [C.F.R. (1982) 40:|50] uses a
high volume sampler (h1-vol) for sample collection and atomic absorption spectrometry for
analysis. The reference method may be revised to require collection of a specific size frac-
tion of atmospheric particles. Size specific Inlets will be discussed in Section 4.2.3.
Airborne lead originates principally from man-made sources, about 75 to 90 percent from
automobile exhaust, and is transported through the atmosphere to vegetation, soil, water, and
animals. Knowledge of environmental concentrations of lead and the extent of its movement
among various media is essential to control lead pollution and to assess its effects on human
populations.
The collection and analysis of environmental samples for lead require a rigorous quality
assurance program [C.F.R. (1982) 40:§58], It is essential that the investigator recognize all
sources of contamination and use every precaution to eliminate them. Contamination occurs on
the surfaces of collection containers and devices, on the hands and clothing of the investi-
gator, in the chemical reagents, in the laboratory atmosphere, and on the labware and tools
used to prepare the sample for analysis. General procedures for controlling contamination in
trace metal analysis are described by Zief and Mitchell (1976). Specific details for the
analysis of lead are given in Patterson and Settle (1976). In the following discussion of
methods for sampling and analysis, it 1s assumed that all procedures are normally carried out
with precise attention to contamination control.
In the following sections, the specific operation, procedure and Instrumentation involved
In monitoring and analyzing environmental lead are discussed. Site selection criteria are
treated briefly due to the lack of verifying data. Much remains to be done in establishing
valid criteria for sampler location. The various types of samples and substrates used to col-
lect airborne lead are described. Methods for collecting dry deposition, wet deposition,
aqueous, soil and vegetation samples are also reviewed along with current sampling methods
specific to mobile and stationary sources. Finally, advantages and limitations of techniques
for sample preparation and analysis are discussed.
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Cascade impactors typically have 2 to 10 stages, and flowrates for commercial low-volume
versions range from about 0.01 to 0.10 m3/m1n. Lee and Goranson (1972) nodified a commer-
cially available 0.03 mVmin low-volume impactor and operated it at 0.14 m3/min to obtain
larger mass collections on each stage. Cascade impactors have also been designed to mount on
a hi-vol sampler and operate at flowrates as high as 0.6 to 1.1 m3/min.
Particle size cutpoints for each stage depend primarily on sampler geometry and flowrate.
The smallest particle size cutpoint routinely used is approximately 0.3 (jib, although special
low-pressure impactors such as that described by Hering et al. (1978) are available with cut-
points as small as 0.05 pm. However, due to the low pressure, volatile organics and nitrates
are lost during sampling. A membrane filter is typically used after the last stage to collect
the remaining small particles.
4.2.2.4 Dry Deposition Sampling. Dry deposition may be measured directly with surrogate or
natural surfaces, or indirectly using micrometeorological techniques. The earliest surrogate
surfaces were dustfall buckets placed upright and exposed for several days. The HASL wet-dry
collector is a modification which permits one of a pair of buckets to remain covered except
during rainfall. These buckets do not collect a representative sample of particles in the
small size range where lead is found because the rim perturbs the natural turbulent flow of
the main airstream (Hicks et al., 1980). They are widely used for other pollutants, espe-
cially large particles, in the National Atmospheric Deposition Program.
Other surrogate surface devices with smaller rims or no rims have been developed recently
(Elias et al., 1976; Lindberg et al., 1979; Peirson et al., 1973). Peirson et al. (1973)
used horizontal sheets of filter paper exposed for several days with protection from rainfall.
Elias et al. (1976) used Teflon® disks held rigid with a 1 cm Teflon® ring. Lindberg et al.
(1979) used petri dishes suspended in a forest canopy. In all of these studies, the calcu-
lated deposition velocity (see Section 6.3.1) was within the range expected for small aerosol
particles.
A few studies have measured direct deposition on vegetation surfaces using chemical wash-
ing techniques to remove surface particles. These determinations are generally 4 to 10 times
lower than comparable surrogate surface measurements (Elias et al., 1976; Lindberg et al.,
1979), but the reason for this difference could be that natural surfaces represent net accumu-
lation rather than total deposition. Lead removed by rain or other processes would show an
apparently lower deposition rate.
There are several micrometeorological techniques that have been used to measure particle
deposition. They overcome the major deficiency of surrogate surfaces, the lack of correlation
between the natural and artificial surfaces, but micrometeorological techniques require expen-
sive equipment and skilled operators. They measure instantaneous or short-term deposition
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TABLE 4-1. DESIGN OF NATIONAL AIR MONITORING STATIONS
Criteria
TSP (Final Rule)
Air Pb (Final Rule)
Spatial scale
Category (a)
Category (b)
Number required
Category (a)
Meters from edge of
roadway
meters above ground
level
Category (b)
Meters from edge of
Meters above ground
Stations required
Neighborhood scale
As per Table 4-2
Siting
Nigh traffic and
population density
neighborhood scale
—" >3000
As per Figure 4-1
2-15
roadway
level
Microscale or middle scale
Neighborhood scale
Minilium 1 each category
where population >500,000
Major roadway
microscale
—550,600
5-15
2-7
or
Major roadway
middle scale
ao.ooo 20,000
>15-50 >15-75 >15-100
2-15
2-15 2-15
High traffic and population density
neighborhood scale
§10,000 20,000 MO, 000
>50 >75 >100
2-15 2-15 2-15
Source: C.F.R. (1982) 40:§58 App E
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PRELIMINARY ORAFT
directly in the stack or exhaust stream. In the tentative ASTW method for sampling for atmos-
pheric lead, air is pulled through a 0.45 h" membrane filter and an activated carbon adsorp-
tion tube (American Society for Testing and Materials, 1975a). In a study of manual methods
for measuring emission concentrations of lead and other toxic materials, Coulson et al.
(1973), recommended use of a filter, a system of impingers, a metering system, and a pump.
4.2.3.2 Mobile Sources. Three principal procedures have been used to obtain samples of auto
exhaust aerosols for subsequent analysis for lead compounds: a horizontal dilution tunnel,
plastic sample collection bags and a low residence time proportional sampler. In each proce-
dure, samples are air diluted to simulate roadside exposure conditions. In the most commonly
used procedure, a large horizontal air dilution tube segregates fine combustion-derived parti-
cles from larger lead particles ablated from combustion chamber and exhaust deposits. In this
procedure, hot exhaust is ducted into a 56-cm diameter, 12-m long, air dilution tunnel and
mixed with filtered ambient air in a 10-cm diameter mixing baffle in a concurrent flow
arrangement. Total exhaust and dilution airflow rate is 28 to 36 iVmin, which produces a
residence time of approximately 5 sec in the tunnel. At the downstream end of the tunnel,
samples of the aerosol are obtained by means of Isokinetic probes using filters or cascade
impaetors (Habibi, 1970).
In recent years, various configurations of the horizontal air dilution tunnel have been
developed. Several dilution tunnels have been made of polyvinyl chloride with a diameter of
46 cm, but these are subject to wall losses due to charge effects (Gentel et al., 1973; Moran
et al., 1972; Trayser et al., 1975). Such tunnels of varying lengths have been limited by
exhaust temperatures to total flows above approximately 11 m3/m1n. Similar tunnels have a
centrifugal fan located upstream, rather than a positive displacement pump located downstream
(Trayser et al., 1975). This geometry produces a slight positive pressure in the tunnel and
expedites transfer of the aerosol to holding chambers for studies of aerosol growth. However,
turbulence from the fan may affect the sampling efficiency. Since the total exhaust plus
dilution airflow is not held constant in this system, potential errors can be reduced by main-
taining a very high dilution air/exhaust flow ratio (Trayser et al., 1975).
There have also been a number of studies using total filtration of the exhaust stream to
arrive at material balances for lead with rather low back-pressure metal filters in an air
distribution tunnel (Habibi, 1973; Hirschler et al., 1957; Hirschler and Gilbert, 1964;
Sampson and Springer, 1973). The cylindrical filtration unit used in these studies is better
than 99 percent efficient in retaining lead particles (Habibi, 1973). Supporting data for
lead balances generally confirm this conclusion (Kunz et al., 1975).
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1*3
ot
ZONE C (UNACCEPTABLE)
ZONE A (ACCEPTABLE
ZONE B (NOT RECOMMENDED)
¦Vl
o
00
u
10 20 25 30
DISTANCE FROM EDGE OF NEAREST TRAFFIC LANE, nwtm
Figure 4-1. Acceptable zone for siting TSP monitors where the average daily traffic exceeds 3000
vehicles/day.
Zone A: Recommended for neighborhood, urban, regional and most middle spatial scales. AN NAMS are In this zona.
Zone B; If SLAMS are placed in Zone B they have middle scale of representativeness.
Source: 48 FR 4415S-44172
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PRELIMINARY DRAFT
4.2.4.2 Surface Water. Atmospheric lead may be dissolved in water as hydrated ions, chemical
complexes, and soluble compounds, or it nay be associated with suspended matter. Because the
physicochemical fern often influences environmental effects, there is a need to differentiate
among the various ehenical forms of lead. Complete differentiation among all such forms is a
complex task that has not yet been fully accomplished. The most commonly used approach is to
distinguish between dissolved and suspended forms of lead. All lead passing through a 0.45 pm
membrane filter is operationally defined as dissolved, while that retained on the filter is
defined as suspended (Kopp and NcKee, 1979).
When sampling water bodies, flow dynamics should be considered in the context of the pur-
pose for which the sample is collected. Water at the convergence point of two flowing
streams, for example, may not be well mixed for several hundred meters. Similarly, the heavy
metal concentrations above and below the thermocline of a lake nay be very different. Thus,
several samples should be selected in order to define the degree of horizontal or vertical
variation. The final sampling plan should be based on the results of pilot studies. In cases
where the average concentration is of primary concern, samples can be collected at several
points and then mixed to obtain a composite.
Containers used for sample collection and storage should be fabricated from essentially
lead-free plastic or glass, e.g., conventional polyethylene, Teflon8, or quartz. These con-
tainers must be leached with hot acid for several days to ensure minimum lead contamination
(Patterson and Settle, 1976). If only the total lead is to be determined, the sample may be
collected without filtration 1n the field. Nitric acid should be added immediately to reduce
the pH to less than 2 (U.S. Environmental Protection Agency, 1978). The acid will normally
dissolve the suspended lead. Otherwise, it is recommended that the sample be filtered upon
collection to separate the suspended and dissolved lead and the latter preserved by acid addi-
tion as above. It 1s also recommended that water samples be stored at 4°C until analysis to
avoid further leaching from the container wall (Fishman and Erdmann, 1973; Kopp and Kroner,
1967; Lovering, 1976; National Academy of Sciences, 1972; U.S. Environmental Protection
Agency, 1978).
4.2.4.3 Soils. The distance and depth gradients associated with lead in soil from emission
sources must be considered in designing the sampling plan. Beyond that, actual sampling is
not particularly complex (Skogerboe et al., 1977b). Vegetation, Utter, and large objects
such as stones should not be included in the sample. Depth samples should be collected at 2
cm intervals to preserve vertical Integrity. The samples should be air dried and stored in
sealed containers until analyzed.
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TABLE 4-3. DESCRIPTION OF SPATIAL SCALES OF REPRESENTATIVENESS
Microscale
Defines ambient concentrations in air volumes associated
.
with areas ranging from several to 100 meters in size.
Middle Scale
Defines concentrations in areas from 100 to 500 meters
(area up to several city blocks).
Neighborhood Scale
Defines concentrations in an extended area of uniform
land use, within a city, from 0.5 to 4.0 kilometers in
size.
Urban Scale
Defines citywide concentrations, areas from 4-50
kilometers in size. Usually requires more than one
site.
Regional Scale
Defines concentrations in a rural area with homogeneous
geography. Range of tens to hundreds of kilometers.
kational and Global
Defines concentrations characterizing the U.S. and the
Scales
globe as a whole.
Source: C.F.R. (1982) 40:§58 App.
D
TABLE 4-4. RELATIONSHIP BETWEEN MONITORING OBJECTIVES AND
APPROPRIATE SPATIAL SCALES
Monitoring objective
Appropriate spatial scale for siting air monitors
Highest Concentration
Micro, Middle, Neighborhood (sometimes Urban).
Population
Neighborhood, Urban
Source Impact
Micro, Middle, Neighborhood
General (Background)
Neighborhood, Regional
Source: C.F.R. (1982) 40:§58 App.
D
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sample collected is large, then the effects of these trace contaminants nay be negligible
(Witz and MacPhee, 1976). Procedures for cleaning filters to reduce the lead blank rely on
washing with acids or complexing agents (Gandrud and Lazrus, 1972). The type of filter and
the analytical method to be used often determines the ashing technique. In some methods,
e.g., X-ray fluorescence, analysis can be performed directly on the filter if the filter
material is suitable (Dzubay and Stevens, 1975). Skogerboe (1974) provided a general review
of filter materials.
The main advantages of glass fiber filters are low pressure drop and high particle col-
lection efficiency at high flow rates. The main disadvantage is variable lead blank, which
makes their use inadvisable in many cases (Kometani et al., 1972; Luke at al., 1972). This
has placed a high priority on the standardization of a suitable filter for hi-vol samples
(Witz and MacPhee, 1976). Other investigations have indicated, however, that glass fiber
filters are now available that do not present a lead interference problem (Scott et al.,
1976b). Teflon* filters have been used since 1975 by Dzubay et al. (1982) and Stevens et al.
(1978), who have shown these filters to have very low lead blanks (<2 ng/cm2). The collection
efficiencies of filters, and also of impactors, have been shown to be dominant factors in the
quality of the derived data (Skogerboe et al., 1977a).
Sample preparation usually involves conversion to a solution through wet ashing of solids
with acids or through dry ashing In a furnace followed by acid treatment. Either approach
works effectively if used properly (Kometani et al., 1972; Skogerboe et al., 1977b). In one
investigation of porous plastic Nuclepore® filters, some lead blanks were too high to allow
measurements of ambient air lead concentrations (Skogerboe et al., 1977b).
4.3 ANALYSIS
The choice of analytical method depends on the nature of the data required, the type of
sample being analyzed, the skill of the analyst, and the equipment available. For general
determination of elemental lead, atomic absorption spectroscopy is widely used and recommended
[40 C.F.R. (1982) 40:§50]. Optical emission spectrometry (Scott et al., 1976b) and X-ray
fluorescence (Stevens et al., 1978) are rapid and inexpensive methods for multlelemental
analyses. X-ray fluorescence can measure lead concentrations reliably to 1 ng/ma using sam-
ples collected with commercial dichotomous samplers. Other analytical methods have specific
advantages appropriate for special studies. Only those analytical techniques receiving wide-
spread current use in lead analysis are described below. More complete reviews are available
in the literature (American Public Health Association, 1971; Lovering, 1976; Skogerboe et al.,
1977b; National Academy of Sciences, 1980).
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Teflon® membrane filters with pore sizes as large as 2.0 can be used In the dichoto-
nous sampler (Dzubay et al, 1982; Stevens et al., 1980) and have been shown to have essen-
tially 100 percent collection efficiency for particles with an aerodynamic diameter as small
as 0.03 y* (Liu et al., 1976; See Section 4.2.5). Because the sampler operates at a flowrate
of 1 ffls/hr (167 1/min) and collects sub-milligram quantities of particles, a microbalance with
a 1 MS resolution is recommended for filter weighing (Shaw, 1980). Removal of the fine par-
ticles via this fractionation technique may result in some of the collected coarse particles
falling off the filter if care is not taken during filter handling and shipping. However,
Dzubay and Barbour (1983) have developed a filter coating procedure which eliminates particle
loss during transport. A study by Wedding et al. (1980) has shown that the Sierra® inlet to
the dichotomous sampler was sensitive to windspeed. The 50 percent cutpoint (D8a) was found
to vary from 10 to 22 m» over the windspeed range of 0 to 15 km/hr.
Automated versions of the sampler allow timely and unattended changes of the sampler
filters. Depending on atmospheric concentrations, short-term samples of as little as 4 hours
can provide diurnal pattern information. The mass collected during such short sample periods,
however, is extremely small and highly variable results may be expected.
4.2.2.3 Impactor Samplers. Impactors provide a means of dividing an ambient particle sample
into subfractlons of specific particle size for possible use in determining size distribution.
A jet of air is directed toward a collection surface, which is often coated with an adhesive
or grease to reduce particle bounce. Large, high-inertia particles are unable to turn with
the airstream and consequently hit the collection surface. Smaller particles follow the air-
stream and are directed toward the next impactor stage or to the filter. Use of multiple
stages, each with a different particle size cutpoint, provides collection of particles in
several size ranges.
For determining particle mass, removable impaction surfaces may be weighed before and
after exposure. The particles collected may be removed and analyzed for individual elements.
The selection and preparation of these Impaction surfaces have significant effects on the
impactor performance. Improperly coated or overloaded surfaces can cause particle bounce to
lower stages resulting in substantial cutpoint shifts (Dzubay et al., 1976). Additionally,
coatings may cause contamination of the sample. Harple and Willeke (1976) showed the effect
of various impactor substrates on the sharpness of the stage cutpoint. Glass fiber substrates
can also cause particle bounce or particle interception (Dzubay et al., 1976) and are subject
to the formation of artifacts, due to reactive gases Interacting with the glass fiber, similar
to those on hi-vol sampler filters (Stevens et al., 1978).
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Pachuta and Love (1980) collected particles on cellulose acetate filters. Disks (0.5
cm2) were punched from these filters and analyzed by insertion of the nichrome cups containing
the disks into a flame. Another application involves the use of graphite cups as particle
filters with the subsequent analysis of the cups directly in the furnace system (Seeley and
5kogerboe, 1974; Torsi et al., 1981). These two procedures offer the ability to determine
particulate lead directly with minimal sample handling.
In an analysis using AAS and hi-vol samplers, atmospheric concentrations of lead were
3
found to be 0.076 ng/in at the South Pole (Maenhaut et al., 1979). Lead analyses of 995 par-
ticulate samples from the NASN were accomplished by AAS with an indicated precision of 11
percent (Scott et al., 1976a, see also Section 7.2.1.1). More specialized AAS methods for the
determination of tetraalkyl lead compounds in water and fish tissue have been described by
Chau et al. (1979) and in air by Birnie and Noden (1980) as well as Rohbock et al. (1980).
Atomic absorption requires as much care as other techniques to obtain highly precise
data. Background absorption, chemical interference, background light loss, and other factors
can cause errors. A major problem with AAS is that untrained operators use it in many labor-
atories without adequate quality control.
Techniques for AAS are still evolving. An alternative to the graphite furnace, evaluated
by Jin and Taga (1982), uses a heated quartz tube through which the metal ion in gaseous
hydride form flows continuously. Sensitivities were 1 to 3 ng/g for lead. The technique is
similar to the hydride generators used for mercury, arsenic, and selenium. Other nonflame
atonization systems, electrodeless discharge lamps, and other equipment refinements and tech-
nique developments have been reported (Horlick, 1982).
4.3.2 Emission Spectroscopy
Optical emission spectroscopy is based on the measurement of the light emitted by
elements when they are excited in an appropriate energy medium. The technique has been used
to determine the lead content of soils, rocks, and minerals at the 5 to 10 pg/g level with a
relative standard deviation of 5 to 10 percent (Anonymous, 1963); this method has also been
applied to the analysis of a large number of air samples (Scott et al., 1976b; Sugimae and
Skogerboe, 1978). The primary advantage of this method is that it allows simultaneous meas-
urement of a large number of elements in a small sample (Ward and Fishman, 1976).
In a study of environmental contamination by automotive lead, sampling times were short-
ened by using a sampling technique in which lead-free porous graphite was used both as the
filter medium and as the electrode in the spectrometer (Copeland et al., 1973; Seeley and
Skogerboe, 1974). Lead concentrations of 1 to 10 pg/*3 were detected after a half-hour flow
at 800 to 1200 ml/min through the filter.
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only, and this deposition is inferred to be to a plane projected surface area only, not neces-
sarily to vegetation surfaces.
Of the five micrometeorological techniques commonly used to measure particle deposition,
only two have been used to measure lead particle deposition. Everett et al. (1979) used the
profile gradient technique by which lead concentrations are measured at two or more levels
within 10 in above the surface. Parallel meteorological data are used to calculate the net
flux downward. Droppo (1980) used eddy correlation, which measures fluctuations in the ver-
tical wind component with adjacent measurements of lead concentrations. The calculated dif-
ferences of each can be used to determine the turbulent flux. These two micrometeorological
techniques and the three not yet used for lead, modified Bowen, variance, and eddy accumula-
tion. are described in detail in Hicks et al, (1980).
4.2.2.5 Gas Collection. When sampling ambient lead with systems employing filters, it is
likely that vapor-phase organolead compounds will pass through the filter media. The use of
bubblers downstream of the filter containing a suitable reagent or absorber for collection of
these compounds has been shown to be effective (Purdue et al., 1973). Organolead may be col-
lected on iodine crystals, adsorbed on activated charcoal, or absorbed in an iodine mono-
chloride solution (Skogerboe et al., 1977b).
In one experiment, Purdue et al. (1973) operated two bubblers In series containing iodine
monochloride solution. One hundred percent of the lead was recovered in the first bubbler.
It should be noted, however, that the analytical detection sensitivity was poor. In general,
use of bubblers limits the sample volume due to losses by evaporation and/or bubble carryover.
4.2.3 Source Sampling
Sources of lead include automobiles, smelters, coal-burning facilities, waste oil combus-
tion, battery manufacturing plants, chemical processing plants, facilities for scrap proces-
sing, and welding and soldering operations (see Section 5.3.3). A potentially Important
secondary source is fugitive dust from mining operations and from soils contaminated with
automotive emissions (Olson and Skogerboe, 1975). Chapter 5 contains a complete discussion of
sources of lead emissions. The following sections discuss the sampling of stationary and
mobile sources.
4.2.3.1 Stationary Sources. Sampling of stationary sources for lead requires the use of a
sequence of samplers at the source of the effluent stream. Since lead in stack emissions may
be present in a variety of physical and chemical forms, source sampling trains must be de-
signed to trap and retain both gaseous and particulate lead. A sampling probe is inserted
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PRELIMINARY DRAFT
bombardment for excitation was demonstrated by Johansson et al. (1970), who reported an Inter-
ference-free signal in the picograa (10 12 g) range. The excellent capability of accelerator
beams for X-ray emission analysis 1s partially due to the relatively low background radiation
associated with the excitation. The high particle fluxes obtainable from accelerators also
contribute to the sensitivity of the PIXE method. Literature reviews (Folkmann et al., 1974;
Gi If rich et al., 1973; Herman et al., 1973; Walter et al., 1974) on approaches to X-ray
elemental analysis agree that protons of a few Me¥ energy provide a preferred combination for
high sensitivity analysis under conditions less subject to matrix interference effects. As a
result of this premise, a system designed for routine analysis has been described (Johansson
et al., 1975) and papers involving the use of PIXE for aerosol analysis have appeared (Hardy
et al., 1976; Johansson et al., 1975). The use of radionuclides to excite X-ray fluorescence
and to determine lead in airborne particles has also been described (Havranek and Bumbalova,
1981; Havranek et al., 1980).
X-radiation is the basis of the electron microprobe method of analysis. When an intense
electron beam is incident on a sample, it produces several forms of radiation, including
X-rays, whose wavelengths depend on the elements present in the material and whose Intensities
depend on the relative quantities of these elements. An electron beam that gives a spot size
as small as 0.2 (jm is possible. The microprobe is often incorporated in a scanning electron
microscope that allows precise location of the beam and comparison of the sample morphology
with Its elemental composition. Under ideal conditions, the analysis is quantitative, with an
accuracy of a few percent. The mass of the analyzed element may range from 10 14 to 10 18 g
(McKinley et al., 1966).
Electron microprobe analysis is not a widely applicable monitoring method. It requires
expensive equipment, complex sample preparation procedures, and a highly trained operator.
The method is unique, however, in providing compositional information on individual lead par-
ticles, thus permitting the study of dynamic chemical changes and perhaps allowing improved
source identification.
Advantages of X-ray fluorescence methods include the ability to detect a variety of
elements, the ability to analyze with little or no sample preparation, low detection limits (2
ng Pb/ma) and the availability of automated analytical equipment. Disadvantages are that the
X-ray analysis requires liquid nitrogen (e.g., for energy-dispersive models) and highly
trained analysts. The detection limit for lead is approximately 9 ng/cm2 of filter area
(Jaklevic and Walter, 1977), which is well below the quantity obtained in normal sampling
periods with the dichotomous sampler (Dzubay and Stevens, 1975).
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In the bag technique, auto emissions produced during simulated driving cycles are air-
diluted and collected in a large plastic bag. The aerosol sample is passed through a filtra-
tion or impaction sampler prior to lead analysis (Ter Haar et a1., 1972). This technique may
result in errors of aerosol size analysis because of condensation of low vapor pressure
organic substances onto the lead particles.
To minimize condensation problems, a third technique, a low residence time proportional
sampling system, has been used. It is based on proportional sampling of raw exhaust, again
diluted with ambient air followed by filtration or impaction (Ganley and Springer, 1974;
Sampson and Springer, 1973). Since the sample flow must be a constant proportion of the total
exhaust flow, this technique may be limited by the response time of the equipment to operating
cycle phases that cause relatively small transients in the exhaust flow rate.
~•2.4 Sanpling for Lead in Other Media
Other primary environmental media that may be affected by airborne lead include precipi-
tation, surface water, soil, vegetation, and foodstuffs. The sampling plans and the sampling
methodologies used in dealing with these media depend on the purpose of the experiments, the
types of measurements to be carried out, and the analytical technique to be used. General
approaches are given below in lieu of specific procedures associated with the numerous possi-
ble special situations.
4.2.4.1 Precipitation. The investigator should be aware that dry deposition occurs continu-
ously, that lead at the start of a rain event is higher in concentration than at the end, and
that rain striking the canopy of a forest may rinse dry deposition particles from the leaf
surfaces. Rain collection systems should be designed to collect precipitation on an event
basis and to collect sequential samples during the event. They should be tightly sealed from
the atmosphere before and after sampling to prevent contamination from dry deposition, falling
leaves, and flying insects. Samples should be acidified to pH 1 with nitric acid and refrig-
erated immediately after sampling. All collection and storage surfaces should be thoroughly
cleaned and free of contamination.
Two automated systems have been in use for some time. The Sangamo Precipitation
Collector, Type A, collects rain in a single bucket exposed at the beginning of the rain event
(Samant and Vaidya, 1982). These authors reported no leaching of lead from the bucket into a
solution of 0.3N HN03. A second sampler, described by Coscio et al. (1982), also remains
covered between rain events; it can collect a sequence of eight samples during the period of
rain and may be fitted with a refrigeration unit for sample cooling. No reports of lead
analyses were given. Because neither system is widely used, their monitoring effectiveness
has not been thoroughly evaluated.
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electrochemical methods generally offer sufficient analytical sensitivity for most lead mea-
surement problems. Differential pulse polarography (DPP) relies on the measurement of the
faradaic current for lead as the voltage is scanhid"While compensating for the nonfaradaic
(background) current produced (McDonnell, 1981). Anodic stripping voltammetry (ASV) is a two
step process in which the lead is preconcentrated onto a mercury electrode by an extended but
selected period of reduction. After the reduction step, the potential is scanned either
linearly or by differential pulse to oxidize the lead and allow measurement of the oxidation
(stripping) current. The preconcentration step allows development of enhanced analytical
signals; when used in combination with the differential pulse method lead concentrations at
the subnanogram level can be measured (Florence, 1980).
The ASV method has been widely applied to the analysis of atmospheric lead (Harrison et
al., 1971; Khandekar et al., 1981; MacLeod and Lee, 1973). Landy (1980) has shown the applic-
ability to the determination of Cd, Cu, Pb, and Zn in Antarctic snow while Nguyen et al.
(1979) have analyzed rain water and snow samples. Green et al. (1981) have used the method to
determine Cd, Cu, and Pb in sea water. The ASV determination of Cd, Cu, Pb, and Zn in foods
has been described by Jones et al., 1977; Mannino, 1982; and Satzger et al., 1982, and the
general accuracy of the method summarized by Holak (1980). Current practice with commercially
available equipment allows lead analysis at subnanogram concentrations with precision at the 5
to 10 percent on a routine basis (Skogerboe et al., 1977b). New developments center around
the use of microcomputers in controlling the stripping voltage (Kryger, 1981) and conforma-
tional modifications of the electrode (Brihaye and Duyckaerts, 1982).
*.3.7 Methods for Compound Analysis
The majority of analytical methods are restricted to measurement of total lead and cannot
directly identify the various compounds of lead. The electron microprobe and other X-ray
fluorescence methods provide approximate data on compounds on the basis of the ratios of
elements present (Ter Haar and Bayard, 1971). Gas chromatography (GC) using the electron cap-
ture detector has been demonstrated to be useful for organolead compounds (Shapiro and Frey,
1968). The use of atomic absorption as the GC detector for organolead compounds has been
described by DeJonghe et al. (1981), while a plasma emission detector has been used by Estes
et al. (1981). In addition, Messman and Rains (1981) have used liquid chromatography with an
atomic absorption detector to measure organolead compounds. Mass spectrometry may also be
used with gas chromatography (Itykytiuk et al., 1980).
Powder X-ray diffraction techniques have been applied to the identification of lead com-
pounds in soils by Olson and Skogerboe (197S) and by Linton et al. (1980). X-ray diffraction
techniques were used (Harrison and Perry, 1977; Foster and Lott, 1980; Jacklevic et al., 1981)
to identify lead compounds collected on air filters.
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4.2.4.4 Vegetation. Because most soil lead is in forms unavailable to plants, and because
lead is not easily transported by plants, roots typically contain very little lead and shoots
even less (Zimdahl, 1976; Zimdahl and Koeppe, 1977). Before analysis, a decision must be made
as to whether or not the plant material should be washed to remove surface contamination from
dry deposition and soil particles. If the plants are sampled for total lead content (e.g., if
they serve as animal food sources), they cannot be washed. If the effect of lead on internal
plant processes is being studied, the plant samples should be washed. In either case, the
decision must be made at the time of sampling, as washing cannot be effective after the plant
materials have dried. Fresh plant samples cannot be stored for any length of time in a
tightly closed container before washing because molds and enzymatic action may affect the dis-
tribution of lead on and in the plant tissues. Freshly picked leaves stored in sealed poly-
ethylene bags at room temperature generally begin to decompose in a few days. Storage time
may be increased to approximately 2 weeks by refrigeration.
After collection, plant samples should be dried as rapidly as possible to minimize chem-
ical and biological changes. Samples that are to be stored for extended periods of time
should be oven dried to arrest enzymatic reactions and render the plant tissue amenable to
grinding. Storage in sealed containers is required after grinding. For analysis of surface
lead, fresh, intact plant parts are agitated in dilute nitric acid or EDTA solutions for a few
seconds.
4.2.4.5 Foodstuffs. From 1972 to 1978, lead analysis was included in the Food and Drug
Administration Market Basket Survey, which involves nationwide sampling of foods representing
the average diet of an 18-year-old male, i.e., the individual who on a statistical basis eats
the greatest quantity of food (Kolbye et al., 1974). Various food items from the several food
classes are purchased in local markets and made up into meal composites in the proportion that
each food item 1s ingested; they are then cooked or otherwise prepared as they would be con-
sumed. Foods are grouped into 12 food classes, then composited and analyzed chemically.
Other sampling programs may be required for different investigative purposes. For those foods
where lead may be deposited on the edible portion, the question of whether or not to use
typical kitchen washing procedures before analysis should be considered in the context of the
experimental purpose.
4.2.5 Filter Selection and Sample Preparation
In sampling for airborne lead, air 1s drawn through filter materials such as glass fiber,
cellulose acetate, or porous plastic (Skogerboe et al., 1977b, Stern, 1968). These materials
often include contaminant lead that can Interfere with the subsequent analysis (Gandrud and
Lazrus, 1972; Koraetani et al. 1972; Luke et al., 1972; Seeley and Skogerboe, 1974). If the
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4.5 REFERENCES
I
American Public Health Association. (1971) Standard methods for the examination of water and
wastewater; 13th Ed. New York, NY: American Public Health Association.
American Society for Testing and Materials. (1975a) Standard method for collection and analy-
sis of dustfall (settleable particulates); D 1739-70. Annu. Book ASTM Stand. 1975:
517-521.
American Society for Testing and Materials. (1975b) Tentative method of test for lead in the
atmosphere by co1orimetric dithizone procedure; D 3112-72T. Annu. Book ASTM Stand. 1975:
633-641.
Anonymous. (1963) Official standardized and recommended methods of analysis. Cambridge, MA:
W. Heffer and Sons, Ltd.
Barfoot, K. M.; Mitchell, I. V.; Eschbach, H. L.; Mason, P. I.; Gil boy, W, B. (1979) The anal-
ysis of air particulate deposits using 2 MeV protons. J. Radioanal. Chem. 53: 255-271.
Bertenshaw, M. P.; Gelsthorpe, 0. (1981) Determination of lead in drinking water by atomic-
absorption spectrophotometry with electrothermal atomisation. Analyst (London) 106:
23-31.
Birks, L. S. (1972) X-ray absorption and emission. Anal. Chem. 44: 557R-562R.
Birks, L. S.; Gilfrich, J. V.; Nagel, D. J. (1971) Large-scale monitoring of automobile
exhaust particulates: methods and costs. Washington, 0C: Naval Research Laboratory; NRL
memorandum report 2350. Available from: NTIS, Springfield, VA; AD 738801.
Birnie, S. E.; Noden, F. G. (1980) Determination of tetramethyl- and tetraethyllead vapours in
air following collection on a glass-fibre-iodised carbon filter disc. Analyst (London)
105: 110-118.
Brihaye, C.; Duyckaerts, G. (1982) Determination of traces of metals by anodic stripping volt-
ammetry at a rotating glassy carbon ring-disc electrode. Part I: Method and instrumenta-
tion with evaluation of some parameters. Anal. Chim. Acta 143: 111-120.
C.F.R. (1982) 40:§50; National primary and secondary ambient air quality standards.
C.F.R. (1982) 40:§58; Ambient air quality surveillance.
Chau, Y. K.; Wong, P. T. S.; Bengert, G. A.; Kramar, 0. (1979) Determination of tetraal kyl
lead compounds in water, sediment, and fish samples. Anal. Chem. 51: 186-188.
Chow, T. J.; Earl, J. L.; Bennet, C. F. (1969) Lead aerosols in marine atmosphere. Environ.
Sci. Technol. 3: 737-742.
Chow, T. J.; Patterson, C. C.; Settle, D. (1974) Occurrence of lead in tuna [Letter]. Nature
(London) 251: 159-161.
Compton, R. 0.; Thomas, L. A. (1980) Analysis of air samples for lead and manganese. Tex.
J. Sci. 32: 351-355.
B04REF/A
4-24
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PRELIMINARY DRAFT
With respect to measuring lead without sampling or laboratory contamination, several in-
vestigators have shown that the magnitude of the problem is quite large (Patterson and Settle,
1976; Patterson et al., 1976; Pierce et al., 1976; Patterson, 1982; Skogerboe, 1982). It
appears that the problem may be caused by failure to control the blank or by failure to stan-
dardize Instrument operation (Patterson, 1982; Skogerboe, 1982). The laboratory atmosphere,
collecting containers, and the labware used may be primary contributors to the lead blank pro-
blem (Murphy, 1976; Patterson, 1982; Skogerboe, 1982). Failure to recognize these and other
sources such as reagents and hand contact is very likely to result in the generation of arti-
ficially high analytical results. Samples with less than 100 pg Pb should be analyzed in a
clean laboratory especially designed for the elimination of lead contamination. Moody (1982)
has described the construction and application of such a laboratory at the National Bureau of
Standards.
For many analytical techniques, a preconcentration step is recommended, Leyden and
Wegschelder (1981) have described several procedures and the associated problems with control-
ling the analytical blank. There are two steps to preconcentration. The first is the removal
of organic matter by dry ashing or wet digestion. The second is the separation of lead from
interfering metallic elements by coprecipitation or passing through a resin column. New sepa-
ration techniques are continuously being evaluated, many of which have application to specific
analytical problems. Yang and Yeh (1982) have described a polyacrylamide-hydrous-zirconia
(PHZ) composite ion exchanger suitable for high phosphate solutions. Corsini, et al. (1982)
evaluated a macroreticular acrylic ester resin capable of removing free and inorganically
bound metal ions directly from aqueous solution without prior chelation.
4.3.1 Atomic Absorption Spectroscopy (AAS)
Atomic absorption spectroscopy (AAS) is a widely accepted method for the measurement of
lead in environmental sampling (Skogerboe et al., 1977b). A variety of lead studies using AAS
have been reported (Kometani et al., 1972; Zoller et al., 1974; Huntzicker et al., 1975; Scott
et al., 1976b; Lester et al., 1977; Hirao et al., 1979; Compton and Thomas, 1980; Bertenshaw
and Gelsthorpe, 1981).
The lead atoms in the sample must be vaporized either in a precisely controlled flame or
in a furnace. Furnace systems in AAS offer high sensitivity as well as the ability to analyze
small samples (Lester et al., 1977; Rouseff and Ting, 1980; Stein et al., 1980; Bertenshaw et
al., 1981). These enhanced capabilities are offset in part by greater difficulty in analyti-
cal calibration and by loss of analytical precision.
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PRELIMINARY DRAFT
4.4 CONCLUSIONS
To monitor lead particles in air, collection with the hi-vol and dichotomous samplers arid
analysis by atomic absorption spectrometry and X-ray fluorescence methods have emerged as the
most widely used methods. Sampling with the hi-vol has inherent biases in sampling large par-
ticles and does not provide for fractionation of the particles according to size, nor does it
allow determination of the gaseous (organic) concentrations. Sampling with a dichotomous
sampler provides size information but does not allow for gaseous lead measurements. The size
distribution of lead aerosol particles is important in considering inhalable particulate
matter. To determine gaseous lead, it is necessary to back up the filter with chemical
scrubbers such as a crystalline iodine trap.
X-ray fluorescence and optical emission spectroscopy are applicable to multi-element
analysis. Other analytical techniques find application for specific purposed. The paucity of
data on the types of lead compounds at subnanogram levels in the ambient air is currently
being addressed through development of improved XRF analyzer procedures.
023PB4/A
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PRELIMINARY DRAFT
Scott et al. (1976a) analyzed composited particulate samples obtained with hi-vols for
about 24 elements, including lead, using a direct reading emission spectrometer. Over 1000
samples collected by the NASN in 1970 were analyzed. Careful consideration of accuracy and
precision led to the conclusion that optical emission spectroscopy is a rapid and practical
technique for particle analysis.
More recent activities have focused attention on the inductively coupled plasma (ICP)
system as a valuable means of excitation and analysis (Garbarino and Taylor, 1979; Winge et
al., 1977). The ICP system offers a higher degree of sensitivity with less analytical inter-
ference than is typical of many of the other emission spectroscopic systems. Optical emission
methods are inefficient when used for analysis of a single element, since the equipment is
expensive and a high level of operator training is required. This problem is largely offset
when analysis for several elements is required as is often the case for atmospheric aerosols.
4.3.3 X-Ray Fluorescence (XRF)
X-ray emissions that characterize the elemental content of a sample also occur when atoms
are irradiated at sufficient energy to excite an inner-shell electron (Hammerle and Pierson,
1975; Jaklevic et al., 1973; Skogerboe et al., 1977b; Stevens et al., 1978). This fluores-
cence allows simultaneous identification of a range of elements including lead.
X-ray fluorescence may require a high-energy irradiation source. But with the X-ray
tubes coupled with fluorescers (Jaklevic et al., 1973; Ozubay and Stevens, 1975; Paciga and
Jervis, 1976) very little energy is transmitted to the sample, thus sample degradation is kept
to a minimum (Shaw et al., 1980). Electron beams (McKinley et al., 1966), and radioactive
isotope sources (Kneip and taurer 1972) have been used extensively (Birks et al., 1971; Birks,
1972) as energy sources for XRF analysis. To reduce background interference, secondary fluor-
escers have been employed (Birks et al., 1971; Dzubay and Stevens, 1975). The fluorescent
X-ray emission from the sample may be analyzed with a crystal monochromator and detected with
scintillation or proportional counters (Skogerboe et al., 1977b) or with low-temperature semi-
conductor detectors that discriminate the energy of the fluorescence. The latter technique
requires a very low level of excitation (Dzubay and Stevens, 1975; Toussaint and Boniforti,
1979).
X-ray emission induced by charged-particle excitation (proton-induced X-ray emission or
PIXE) offers an attractive alterative to the more common techniques (Barfoot et al., 1979;
Hardy et al., 1976; Johansson et al., 1970). Recognition of the potential of heavy-particle
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PRELIMINARY DRAFT
4.3.4 Mass Spectrometry
Isotope dilution mass spectrometry (IOMS) is an absolute measurement technique. It
serves as the standard to which other analytical techniques are compared. No other techniques
serve more reliably as a comparative reference. Its use for analyses at subnanogram concen-
trations of lead and in a variety of sample types has been reported (Chow et al., 1969, 1974;
Facchetti and Geiss, 1982; Hirao and Patterson, 1974; Murozumi et al., 1969; Patterson et al.,
1976; Rabinowitz et al., 1973).
The isotopic composition of lead peculiar to various ore bodies and crustal sources may
also be used as a means of tracing the origin of anthropogenic lead. Other examples of IDMS
application are found in several reports cited above, and in Rabinowitz and Wetherill (1972),
Stacey and Kramers (1975), and Machi an et al. (1976).
4.3.5 Colorinetric Analysis
Colorimetric or spectrophotometry analysis for lead using dithizone (diphenylthiocarba-
zone) as the reagent has been used for many years (Anonymous, 1963; Horowitz et al., 1970;
Sandell, 1944). It was the primary method recommended by a National Academy of Sciences
(1972) report on lead, and the basis for the tentative method of testing for lead in the
atmosphere by the American Society for Testing and Materials (1975b). Prior to the
development of the IDMS method, colorinetric analysis served as the reference by which other
methods were tested.
The procedures for the colorinetric analysis require a skilled analyst if reliable
results are to be obtained. The ASTM conducted a collaborative test of the method (Foster et
al., 1975) and concluded that the procedure gave satisfactory precision in the determination
of particulate lead in the atmosphere. In addition, the required apparatus 1s simple and
relatively inexpensive, the absorption is linearly related to the lead concentration, large
samples can be used, and interferences can be removed (Skogerboe et al., 1977b). Realization
of these advantages depends on meticulous attention to the procedures and reagents.
4.3.6 Electrochemical Methods: Anodic Stripping Voltammetry (ASV), Differential Pulse
Polarography (DPP)
Analytical methods based on electrochemical phenomena are found in a variety of forms
(Sawyer and Roberts, 1974; Willard et al., 1974). They are characterized by a high degree of
sensitivity, selectivity, and accuracy derived from the relationship between current, charge,
potential, and time for electrolytic reactions in solutions. The electrochemistry of lead is
based primarily on Pb(II), which behaves reverslbly 1n ionic solutions having a reduction po-
tential near -0.4 volt versus the standard calomel electrode (Skogerboe et al., 1977b). Two
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Draft
Do Not Quote or Cite
EPA-600/8-83-028A
August 1983
External Review Draft
Air Quality Criteria
for Lead
Volume II of IV
NOTICE
This document is a preliminary draft. It has not bean formally released by EPA and should not at this stage
be construed to represent Agency policy. It is being circulated for comment on its technical accuracy and
policy implications.
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
-------
NOTICE
Mention of trade names or commercial products does not constitute
endorsement or recommendation for use.
11
-------
ABSTRACT
The document evaluates and assesses scientific information on the health
and welfare effects associated with exposure to various concentrations of lead
in ambient air. The literature through 1983 has been reviewed thoroughly for
information relevant to air quality criteria, although the document is not
intended as a complete and detailed review of all literature pertaining to
lead. An attempt has been made to identify the major discrepancies in our
current knowledge and understanding of the effects of these pollutants.
Although this document is principally concerned with the health and
welfare effects of lead, other scientific data are presented and evaluated in
order to provide a better understanding of this pollutant in the environment.
To this end, the document Includes chapters that discuss the chemistry and
physics of the pollutant; analytical techniques; sources, and types of
emissions; environmental concentrations and exposure levels; atmospheric
chemistry and dispersion modeling; effects on vegetation; and respiratory,
physiological, toxicological, clinical, and epidemiological aspects of human
exposure.
111
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PRELIMINARY DRAFT
CONTENTS
Page
VOLUME I
Chapter 1. Executive Summary and Conclusions 1-1
VOLUME II
Chapter 2. Introduction 2-1
Chapter 3. Chemical and Physical Properties 3-1
Chapter 4. Sampling and Analytical Methods for Environmental Lead 4-1
Chapter 5. Sources and Emissions 5-1
Chapter 6. Transport and Transformation 6-1
Chapter 7. Environmental Concentrations and Potential Pathways to Human Exposure .. 7-1
Chapter 8. Effects of Lead on Ecosystems 8-1
VOLUME III
Chapter 9. Quantitative Evaluation of Lead and Biochemical Indices of Lead
Exposure in Physiological Media 9-1
Chapter 10. Metabolism of Lead 10-1
Chapter 11. Assessment of Lead Exposures and Absorption 1n Human Populations 11-1
Volume IV
Chapter 12. Biological Effects of Lead Exposure 12-1
Chapter 13. Evaluation of Human Health Risk Associated with Exposure to Lead
and Its Compounds 13-1
TCPBA/H 1v 7/1/83
I
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PRELIMINARY DRAFT
TABLE OF CONTENTS
Page
2. INTRODUCTION 2-1
3. CHEMICAL AND PHYSICAL PROPERTIES 3-1
3.1 INTRODUCTION 3-1
3.2 ELEMENTAL LEAD 3-1
3.3 GENERAL CHEMISTRY OF LEAD 3-2
3.4 ORGANOMETALLIC CHEMISTRY OF LEAD 3-3
3.5 FORMATION OF CHELATES AND OTHER COMPLEXES 3-4
3.6 REFERENCES 3-8
4. SAMPLING AND ANALYTICAL METHODS FOR ENVIRONMENTAL LEAD 4-1
4.1 INTRODUCTION 4-1
4.2 SAMPLING 4-2
4.2.1 Regulatory Siting Criteria for Ambient Aerosol Samplers 4-2
4.2.2 Ambient Sampling for Particulate and Gaseous Lead 4-6
4.2.2.1 High Volume Sampler (hl-vol) 4-6
4.2.2.2 Dichotomous Sampler 4-8
4.2.2.3 Impactor Samplers 4-9
4.2.2.4 Dry Deposition Sampling 4-10
4.2.2.5 Gas Collection 4-11
4.2.3 Source Sampling 4-11
4.2.3.1 Stationary Sources 4-11
4.2.3.2 Mobile Sources 4-12
4.2.4 Sampling for Lead in Other Media 4-13
4.2.4.1 Precipitation 4-13
4.2.4.2 Surface Water 4-14
4.2.4.3 Soils 4-14
4.2.4.4 Vegetation 4-15
4.2.4.5 Foodstuffs 4-15
4.2.5 Filter Selection and Sample Preparation 4-15
4.3 ANALYSIS 4-16
4.3.1 Atomic Absorption Analysis (AAS) 4-17
4.3.2 Emission Spectroscopy . 4-18
4.3.3 X-Ray Fluorescence (XRF) 4-19
4.3.4 Mass Spectrometry (IDMS) 4-21
4.3.5 Colorimetric Analysis 4-21
4.3.6 Electrochemical Methods: Anodic Stripping Voltammotry
(ASV), and Differential Pulse Polarography (DPP) 4-21
4.3.7 Methods for Compound Analysis 4-22
4.4 CONCLUSIONS 4-23
4.5 REFERENCES 4-24
5. SOURCES AND EMISSIONS 5-1
5.1 HISTORICAL PERSPECTIVE 5-1
5.2 NATURAL SOURCES 5-3
5.3 MANMADE SOURCES 5-5
5.3.1 Production 5-5
5.3.2 Utilization 5-5
5.3.3 Emissions 5-7
5.3.3.1 Mobile Sources 5-7
5.3.3.2 Stationary Sources 5-20
TCPBA/E V 7/1/83
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
Page
5.4 SUMMARY 5-20
5.5 REFERENCES 5-22
6. TRANSPORT AND TRANSFORMATION 6-1
6.1 INTRODUCTION 6-1
6.2 TRANSPORT OF LEAD IN AIR BY DISPERSION 6-2
6.2.1 Fluiff Mechanics of Dispersion 6-2
6.2.2 Influence of Dispersion on Ambient Lead Concentrations 6-4
6.2.2.1 Confined and Roadway Situations 6-4
6.2.2.2 Dispersion of Lead on an Urban Scale 6-6
6.2.2.3 Dispersion from Spelter and Refinery Locations 6-8
6.2.2.4 Dispersion to Regional and Remote Locations 6-8
6.3 TRANSFORMATION OF LEAD IN AIR 6-17
6.3.1 Particle Size Distribution 6-17
6.3.2 Organic (Vapor Phase) Lead In A1r 6-22
6.3.3 Chemical Transformations of Inorganic Lead in Air 6-23
6.4. REMOVAL OF LEAD FROM THE ATMOSPHERE 6-25
6.4.1 Dry Deposition 6-25
6.4.1.1 Mechanisms of dry deposition 6-25
6.4.1.2 Dry deposition models 6-26
6.4.1.3 Calculation of dry deposition 6-27
6.4.1.4 Field measurements of dry deposition on
surrogate natural surfaces 6-29
6.4.2 Wet Deposition 6-30
6.4.3 Global Budget of Atmospheric Lead 6-31
6.5 TRANSFORMATION AND TRANSPORT IN OTHER ENVIRONMENTAL MEDIA 6-33
6.5.1 Soil 6-33
6.5.2 Water 6-37
6.5.2.1 Inorganic 6-37
6.5.2.2 Organic 6-38
6.5.3 Vegetation Surfaces 6-41
6.6 SUMMARY 6-42
6.7 REFERENCES 6-44
7. ENVIRONMENTAL CONCENTRATIONS AND POTENTIAL PATHWAYS TO HUMAN EXPOSURE 7-1
7.1 INTRODUCTION 7-1
7.2 ENVIRONMENTAL CONCENTRATIONS 7-1
7.2.1 Ambient Air 7-1
7.2.1.1 Total Airborne Lead Concentrations 7-3
7.2.1.2 Compliance with the 1978 Air Quality Standard 7-13
7.2.1.3 Changes in Air Lead Prior to Human Uptake 7-13
7.2.2 Lead in Soil 7-24
7.2.2.1 Typical Concentrations of Lead in Soil 7-26
7.2.2.2 Pathways of Soil Lead to Human Consumption 7-28
7.2.3 Lead in Surface and Ground Water 7-32
7.2.3.1 Typical Concentrations of Lead in Untreated Water 7-32
7.2.3.2 Human Consumption of Lead in Water 7-33
7.2.4 Summary of Environmental Concentrations of Lead 7-35
7.3 POTENTIAL PATHWAYS TO HUMAN EXPOSURE 7-36
7.3.1 Baseline Human Exposure 7-37
TCPBA/E v1 7/1/83
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
tm
7.3.1.1 Lead in Inhaled Air 7-39
7.3.1.2 Lead in Food 7-39
7.3.1.3 Lead in Drinking Water 7-47
7.3.1.4 Lead in Dusts 7-50
7.3.1.5 Summary of Baseline Human Exposure to Lead 7-55
7.3.2 Additive Exposure Factors 7-56
7.3.2.1 Special Living and Working Environments 7-56
7.3.2.2 Additive Exposures Due to Age, Sex, or Socioeconomic
Status 7-65
7.3.2.3 Special Habits or Activities 7-65
7.3.3 Summary of Additive Exposure Factors 7-67
7.4 SUMMARY 7-67
8. EFFECTS OF LEAD ON ECOSYSTEMS 8-1
8.1 INTRODUCTION 8-1
8.1.1 Scope of Chapter 8 8-1
8.1.2 Ecosystem Functions 8-4
8.1.2.1 Types of Ecosystems 8-4
8.1.2.2 Energy Flow and Biogeochemical Cycles 8-4
8.1.2.3 Biogeochemistry of Lead 8-7
8.1.3 Criteria for Evaluating Ecosystem Effects 8-8
8.2 LEAD IN SOILS AND SEDIMENTS 8-12
8.2.1 Distribution of Lead in Soils 8-12
8.2.2 Origin and Availability of Lead in Aquatic Sediments 8-13
8.3 EFFECTS OF LEAD ON PLANTS 8-14
8.3.1 Effects on Vascular Plants and Algae 8-14
8.3.1.1 Uptake by Plants 8-14
8.3.1.2 Physiological Effects on Plants 8-17
8.3.1.3 Lead Tolerance in Vascular Plants 8-20
8.3.1.4 Effects of Lead on Forage Crops 8-21
8.3.1.5 Summary of Plant Effects 8-21
8.3.2 Effects on Bacteria and Fungi 8-21
8.3.2.1 Effects on Decomposers 8-21
8.3.2.2 Effects on Nitrifying Bacteria 8-24
8.3.2.3 Methylation by Aquatic Microorganisms 8-24
8.3.2.4 Summary of Effects on Microorganisms 8-24
8.4 EFFECTS OF LEAO ON DOMESTIC AND WILD ANIMALS 8-25
8.4.1 Vertebrates 8-25
8.4.1.1 Terrestrial Vertebrates 8-25
8.4.1.2 Effects on Aquatic Vertebrates 8-27
8.4.2 Invertebrates ; 8-30
8.4.3 Summary of Effects on Animals 8-33
8.5 EFFECTS OF LEAD ON ECOSYSTEMS 8-33
8.5.1 Delayed Decomposition .... 8-34
8.5.2 Circumvention of Calcium Biopurification 8-35
8.5.3 Population Shifts Toward Lead Tolerant Populations 8-37
8.5.4 Mass Balance Distribution of Lead in Ecosystems 8-37
8.6 SUMMARY 8-39
8.7 REFERENCES 8-41
TCPBA/E v11 7/1/83
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PRELIMINARY DRAFT
LIST OF FIGURES
Figure Page
3-1 Metal complexes of lead 3-6
3-2 Softness parameters of metal s 3-6
3-3 Structure of chelating agents 3-7
4-1 Acceptable zone for siting TSP monitors 4-5
5-1 Chronological record of the relative increase of lead in snow strata, pond
and lake sediments, marine sediments, and tree rings 5-2
5-2 The global lead production has changed historically 5-4
5-3 Location of major lead operations in the United States 5-9
5-4 Estimated lead-only emissions distribution per gallon of combusted fuel ...... 5-14
5-5 Trend in lead content of U.S. gasolines, 1975-1982 5-16
5-6 Trend in U.S. gasoline sales, 1975-1982 5-17
5-7 Lead consumed in gasoline and ambient lead concentrations, 1975-1982 5-18
5-8 Relationship between lead consumed in gasoline and composite maximum
quarterly average lead levels, 1975-1980 5-19
6-1 Isopleths are shown for annual average particulate lead in pg/m3 6-7
6-2 Spatial distribution of surface street and freeway traffic in
the Los Angeles Basin (10a VMT/day) for 1979 6-9
6-3 Annual average suspended lead concentrations for 1969 in the
Los Angeles Basin, calculated from the model of Cass (1975) 6-10
6-4 Profile of lead concentrations in the northeast Pacific 6-13
6-5 Midpoint collection location for atmospheric sample collected
from R.V. Trident north of 30% 1970 through 1972 6-14
6-6 The EFcrust values for atmospheric trace metals 6-14
6-7 Lead concentration profile in snow strata of northern Greenland 6-16
6-8 Cumulative mass distribution for lead particles in auto exhaust 6-18
6-9 Particulate lead size distribution measured at the Allegheny
Mountain Tunnel, Pennsylvania Turnpike, 1975 6-19
6-10 Particle size distributions of substances in gutter debris,
Rotunda Drive, Dearborn, Michigan 6-20
6-11 Predicted relationship between particle size and deposition velocity at
various conditions of atmospheric stability and roughness height 6-28
6-12 Variation of lead saturation capacity with cation exchange
capacity in soil at selected pH values 6-36
6-13 Lead distribution between filtrate and suspended solids in
stream water from urban and rural compartments 6-39
7-1 Pathways of lead from the environment to human consumption 7-2
7-2 Percent of urban stations reporting indicated concentration Interval 7-6
7-3 Seasonal patterns and trends quarterly average urban lead concentrations 7-11
7-4 Time trends in ambient air lead at selected urban sites 7-12
7-5 Airborne mass size distributions for lead taken from the literature 7-21
7-6 Paint pigments and solder are two additional sources of potential lead
exposure which are not of atmospheric origin 7-36
7-7 Change 1n drinking water lead concentration is a house with lead
plumbing for the first use of water in the morning. Flushing rate
was 10 liters/minute 7-47
7C-1 Concentrations of lead in air, in dust, and on children's hands, measured
during the third population survey. Values obtained less than 1 km from the
smelter, at 2.5 km from the smelters, and in two control areas are shown 7C-4
7C-2 Schematic plan of lead mine and smelter from Mexa Valley, Yugoslavia study ... 7C-7
8-1 The major components of an ecosystem are the primary producers,
grazers, and decomposers 8-6
TCPBA/F V111 7/1/83
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PRELIMINARY DRAFT
LIST OF FIGURES (continued).
Figure Page
8-2 The ecological success of a population depends in part on the
availability of all nutrients at some optimum concentration 8-10
8-3 This figure attempts to reconstruct the right portion of a
tolerance curve 8-11
8-4 Within the decomposer food chain, detritus is progressively
broken down in a sequence of steps 8-23
8-5 The atomic ratios Sr/Ca, Ba/Ca and Pb/Ca (0) normally
decrease by several 8-36
TCPBA/F 7/1/83
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PRELIMINARY DRAFT
LIST OF TABLES
Table Page
3-1 Properties of elemental lead 3-2
4-1 Design of national air monitoring stations 4-3
4-2 TSP NAMS criteria 4-4
4-3 Description of spatial scales of representativeness .. 4-7
4-4 Relationship between monitoring objectives and
appropriate spatial scales 4-7
5-1 U.S. utilization of lead by product category 5-6
5-2 Estimated atmospheric lead emissions for the U.S., 1981, and the world 5-8
5-3 Light-duty vehicular particulate emissions — 5-11
5-4 Heavy-duty vehicular particulate emissions .... 5-11
5-5 Recent and projected consumption of gasoline lead 5-12
6-1 Summary of microscale concentrations 6-5
6-2 Enrichment of atmospheric aerosols over crustal abundance 6-15
6-3 Comparison of size distributions of lead-containing particles in
major sampl i ng areas 6-21
6-4 Distribution of lead in two size fractions at several sites
in the United States 6-22
6-5 Summary of surrogate and vegetation surface deposition of lead 6-29
6-6 Deposition of lead at the Walker Branch Watershed, 1974 6-31
6-7 Estimated global deposition of atmospheric lead 6-32
7-1 Atmospheric lead in urban, rural and remote areas of the world 7-4
7-2 Cumulative frequency distributions of urban air lead concentrations 7-7
7-3 Air lead concentrations in major metropolitan areas 7-9
7-4 Stations with air lead concentrations greater than 1.0 7-14
7-5 Distribution of air lead concentrations by type of site 7-19
7-6 Vertical distribution of lead concentrations 7-22
7-7 Comparison of indoor and outdoor airborne lead concentrations 7-25
7-8 Summary of soil lead concentrations 7-28
7-9 Background lead in basic food crops and meats 7-28
7-10 Summary of lead in drinking water supplies 7-35
7-11 Summary of environmental concentrations of lead 7-35
7-12 Summary of inhaled air lead exposure 7-39
7-13 Lead concentrations in milk and foods 7-41
7-14 Addition of lead to food products 7-43
7-15 Prehistoric and modern concentrations in human food from a marine food
chain 7-44
7-16 Recent trends of lead concentrations in food items 7-45
7-17 Summary of lead concentrations in milk and foods by source 7-46
7-18 Summary by age and sex of estimated average levels of lead injested from
mi 1 k and foods 7-47
7-19 Summary by source of lead consumed from milk and foods 7-50
7-20 Summary by source of lead concentrations in water and beverages 7-51
7-21 Daily consumption and potential lead exposure from water and beverages 7-52
7-22 Summary by source of lead consumed in water and beverages 7-53
7-23 Current baseline estimates of potential human exposure to dusts 7-55
7-24 Summary of baseline human exposures to lead 7-56
7-25 Summary of potential additive exposures to lead 7-59
8-1 Estimated natural levels of lead in ecosystem 8-11
8-2 Estimates of the degree of contamination of herbivores,
omnivores, and carnivores 8-25
TCPBA/G x 7/1/83
-------
PRELIMINARY ORAFT
LIST OF ABBREVIATIONS
AAS
Ach
ACTH
AOCC
ADP/Q ratio
AIDS
AIHA
All
ALA
ALA-D
ALA-S
ALA-U
APDC
APHA
ASTM
ASV
ATP
fl-eel1s
Ba
BAL
BAP
BSA
BUN
BW
C.V.
CaBP
CaEDTA
CBO
Cd
CDC
CEC
CEH
CFR
CMP
CNS
CO
COHb
CP-U
cBah
D.F.
OA
DCMU
DDP
DNA
OTH
EEC
EEG
EMC
EP
EPA
Atomic absorption spectrometry
Acetylcholine
Adrenocoticotrophic hormone
Antibody-dependent cell-mediated cytotoxicity
Adenosine diphosphate/oxygen ratio
Acquired immune deficiency syndrome
American Industrial Hygiene Association
Angiotensin II
Aminolevulinic acid
Aminolevulinic acid dehydrase
Aminolevulinic acid synthetase
Aminolevulinic acid in urine
Ammonium pyrroli di ne-di thiocarbamate
American Public Health Association
Amercian Society for Testing and Materials
Anodic stripping voltammetry
Adenosine triphosphate
Bone marrow-derived lymphocytes
Bari um
British anti-Lewisite (AKA dimercaprol)
benzo(a)pyrene
Bovine serum albumin
Blood urea nitrogen
Body weight
Coefficient of variation
Calcium binding protein
Calcium ethylenediami netetraacetate
Central business district
Cadmium
Centers for Disease Control
Cation exchange capacity
Center for Environmental Health
reference method
Cytidine monophosphate
Central nervous system
Carbon monoxide
Carboxyhemoglobi n
Urinary coproporphyria
plasma clearance of p-aminohippuric acid
Copper
Degrees of freedom
Dopamine
[3-(3,4-dichlorophenyl)-l,l-dimethylurea
Differential pulse polarography
Deoxyribonucleic acid
Delayed-type hypersensitivity
European Economic Community
E1ectroenceph&logram
Encephalomyocardi ti s
Erythrocyte protoporphyrin
U.S. Environmental Protection Agency
TCPBA/D
xi
7/13/83
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
FA Fulvic acid
FDA Food and Drug Administration
Fe Iron
FEP Free erythrocyte protoporphyrin
FY Fiscal year
G.M. Grand mean
G-6-PD Glucose-6-phosphate dehydrogenase
GABA Gamma-aminobutyric acid
SALT Gut-associated lymphoid tissue
GC Gas chromatography
GFR Glomerular filtration rate
HA Humic acid
Hg Mercury
hi-vol High-volume air sampler
HPLC High-performance liquid chromatography
i.n. Intramuscular (method of injection)
i.p. Intraperitoneally (method of injection)
i. v. Intravenously (method of injection)
IAA Indol-3-ylacetic acid
IARC International Agency for Research on Cancer
ICO International classification of diseases
ICP Inductively coupled plasma
IDMS Isotope dilution mass spectrometry
IF Interferon
ILE Isotopic Lead Experiment (Italy)
IRPC International Radiological Protection Commission
K Potassium
LAI Leaf area index
LDH-X Lactate dehydrogenase isoenzyme x
LC-n Lethyl concentration (50 percent)
LDgft Lethal dose (50 percent)
LH Luteinizing hormone
LIPO Laboratory Improvement Program Office
In National logarithm
LPS Lipopolysaccharide
LRT Long range transport
mRNA Messenger ribonucleic acid
ME Mercaptoethanol
MEPP Miniature end-plate potential
MES Maximal electroshock seizure
MeV Mega-electron volts
MLC Mixed lymphocyte culture
MMD Mass median diameter
MMED Mass median equivalent diameter
Mn Manganese
MNO Motor neuron disease
MSV Moloney sarcoma virus
MTD Maximum tolerated dose
n Number of subjects
N/A Not Available
TCPBA/D X11 7/13/83
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued)
NA Not Applicable
NAAQS National ambient air quality standards
NAOB National Aerometric Data flank
NAMS National Air Monitoring Station
NAS National Academy of Sciences
NASN National Air Surveillance Network
NBS National Bureau of Standards
Ni Norepinephrine
NFAN National Filter Analysis Network
NFR-82 Nutrition Foundation Report of 1982
NHANES II National Health Assessment and Nutritional Evaluation Survey II
N1 Nickel
QSHA Occupational Safety and Health Administration
P Potassium
p Significance symbol
PAH Para-aminohippuric acid
Pb Lead
PBA Air lead
Pb(Ac), Lead acetate
PbB concentration of lead in blood
PbBrCl Lead (II) bromocbloride
P8G Porphobilinogen
PFC Plaque-forming cells
pH Measure of acidity
PHA P hytohenagglutinin
PHZ Polyacrylamide-hydrous-zirconia
PIXE Proton-induced X-ray emissions
PMN Polymorphonuclear leukocytes
PND Post-natal day
PNS Peripheral nervous system
ppm Parts per million
PRA Plasma renin activity
PRS Plasma renin substrate
PVfM Pokeweed mitogen
Py-5-N Pyriwide-5'-nucleotidase
RBC Red blood cell; erythrocyte
RBF Renal blood flow
RCR Respiratory control ratios/rates
redox Oxidation-reduction potential
RES Reticuloendothelial system
RLV Rauscher leukemia virus
RNA Ribonucleic acid
S-HT Serotoni n
SA-7 Simian adenovirus
sea Standard cubic meter
S.D. Standard deviation
SDS Sodium dodecyl sulfate
S.E.M. Standard error of the mean
SES Socioeconomic status
SCOT Serum glutamic oxaloacetic transaminase
TCPBA/D x111 7/13/83
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
slg
SLAMS
SMR
Sr
SRBC
SRMs
STEL
SW voltage
T-cells
t-tests
TBL
TEA
TEL
TIBC
TML
TMLC
TSH
TSP
U.K.
UMP
USPHS
VA
Ih
WHO
XRF
X^
Zn
ZPP
Surface 1mmunoglobulin
State and local air monitoring stations
Standardized mortality ratio
Stronti um
Sheep red blood cells
Standard reference materials
Short-term exposure limit
Slow-wave voltage
Thymus-derived lymphocytes
Tests of significance
Tri-n-butyl lead
T etraethy 1 -amnion i um
Tetraethyllead
Total iron binding capacity
Tetramethyllead
Tetramethyllead chloride
Thyroid-stimulating hormone
Total suspended particulate
United Kingdom
Uridine monophosphate
U.S. Public Health Service
Veterans Administration
Deposition velocity
Visual evoked response
World Health Organization
X-Ray fluorescence
Chi squared
Zinc
Erythrocyte zinc protoporphyrin
MEASUREMENT ABBREVIATIONS
dl deciliter
ft feet
g gran
g/gal gram/gallon
g/ha-mo gram/hectare*nonth
km/hr kilometer/hour
1/min liter/minute
¦g/km milligram/kilometer
Mfl/n3 microgram/cubic meter
mm millimeter
Mi>ol micrometer
ng/cm2 nanograms/square centimeter
ran nanometer
nM nanomole
sec second
TCPBA/D xiY 7/13/83
-------
AUTHORS, CONTRIBUTORS, AND REVIEWERS
Chapter 3: Physical and Chemical Properties of Lead
Principal Author
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 554S5
Dr. Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. William Pierson
Scientific Research Labs,
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Glen Sanderson
University of Illinois
Illinois Natural History Survey
Urbana, IL 61801
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
Baton Rouge, LA 70801
Or. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
XV
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Chapter 4; Sampling and Analytical Methods for Environmental Lead
Principal Authors
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Dr. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80521
Contributing Author
Dr. Robert Bruce
Environmental Criteria and Assessment Office
MO-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. John i. Clements
Environmental Monitoring Systems Laboratory
MD-78
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. Tom Dzubay
Inorganic Pollutant Analysis Branch
MD-47
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Or. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Or. Samuel Lestz
Department of Mechanical
Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H. Liu
Department of Mechanical
Engineering
University of Minnesota
Minneapolis, MM 55455
Dr. Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. Bill Hunt
Monitoring and Data Analysis Division
MD-14
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Glen Sanderson
University of Illinois
Illinois Natural History Survey
Urbana, IL 61801
xv 1
-------
Mr, Stan Sleva
Office of Air Quality Planning and Standards
MO-14
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Or. William H. Sirith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of Forestry
New Haven, CT 06S11
Dr. Robert Stevens
Inorganic Pollutant Analysis Branch
MD-47
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Chapter 5: Sources and Emissions
Principal Author
Or. James Braddock
Mobile Source Emissions Research Branch
MD-46
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Contributing Author
Dr. Tom McMullen
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Dr. Glen Sanderson
University of Illinois
Illinois Natural History Survey
Urbana. IL 61801
Dr. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
xv11
-------
Dr. Ben Y. H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Uale University, School of Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Or. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
Or. Michael Oppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Chapter 6: Transport and Transformation
Principal Author
Dr. Ron Bradow
Mobile Source Emissions Research Branch
MD-46
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Contributing Authors
Dr. Robert Elias Dr. Rodney Skogerboe
Environmental Criteria and Assessment Office Department of Chemistry
MD-52 Colorado State University
U.S. Environmental Protection Agency Fort Collins, CO 80521
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request;
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. Derek Hodgson
Department of Chemistry
University of North Carolina
Chapel Hill, NC 27514
Dr. David E. Koeppe
Department of Plant and Soil Science
Texas Technical University
Lubbock, TX 79409
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, 1L 61801
Dr. Glen Sanderson
Illinois Natural History Survey
University of Illinois
Urbana, IL 61801
xvili
-------
Dr. Samuel testz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Or. Ben Y. H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Dr. Michael Qppenheimer
Environmental Defense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
Chapter 7: Environmental Concentrations and Potential Pathways to Human
Exposure
Principal Authors
Dr. Cliff Davidson
Department of Civil Engineering
Carnegie-Mellon University
Schenley Park
Pittsburgh, PA 15213
Dr. Robert Elias
Environmental Criteria and
Assessment Office
MD-52
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request:
Dr. Carol Angle
Department of Pediatrics
University of Nebraska
College of Medicine
Omaha, NE 68105
Dr. Lee Annest
Division of Health Exaain. Statistics
National Center for Health Statistics
3700 East-West Highway
Hyattsville, MD 20782
Dr. Donald Barltrop
Department of Child Health
Westminister Children's Hospital
London SW1P 2NS
England
Dr. A. C. Chamberlain
Environmental and Medical
Sciences Division
Atomic Energy Research
Establishment
Harwell 0X11
England
Dr. Neil Chernoff
Division of Developmental Biology
MD-67
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Julian Chi solm
Baltimore City Hospital
4940 Eastern Avenue
Baltimore, MD 21224
xix
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Dr. Irv Billick
Gas Research Institute
8600 West Bryn Mawr Avenue
Chicago, IL 60631
Dr. Joe Boone
Clinical Chemistry and
Toxicology Section
Centers for Disease Control
Atlanta, GA 30333
Or. Robert Bornschein
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
Dr. Jack Dean
Inmunobiology Program and
Imaiunotoxicology/Cell Biology program
CIIT
P.O. Box 12137
Research Triangle Park, NC 27709
Or. Fred deSerres
Associate Director for Genetics
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Robert Dixon
Laboratory of Reproductive and
Developmental Toxicology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Claire Ernhart
Department of Psychiatry
Cleveland Metropolitan General Hospital
Cleveland, OH 44109
Or. Sergio Fachettl
Section Head - Isotope Analysis
Chemistry Division
Joint Research Center
121020 Ispra
Varese, Italy
Dr. Virgil Perm
Department of Anatoqy and Cytology
Dartmouth Medical School
Hanover, NH 03755
Mr. Jerry Cole
International Lead-Z1nc Research
Organization
292 Madison Avenue
New York, NY 10017
Dr. Max Costa
Department of Pharmacology
University of Texas Medical
School
Houston, TX 77025
Dr. Anita Curran
Commissioner of Health
Westchester County
White Plains, NY 10607
Dr. Warren Galke
Department of Biostatisties
and Epidemiology
School of Allied Health
East Carolina University
Greenville, NC 27834
Mr. Eric Goldstein
Natural Resources Defense
Council, Inc.
122 E. 42nd Street
New York, NY 10168
Dr. Harvey Gonick
1033 Gayley Avenue
Suite 116
Los Angeles, CA 90024
Dr. Robert Goyer
Deputy Director
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Stanley Gross
Hazard Evaluation Division
Toxicology Branch
U.S. Environmental Protection
Agency
Washington, DC 20460
Dr. Paul Hammond
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
xx
-------
Dr. Alf Fischbein
Environmental Sciences Laboratory
Mt. Sinai School of Medicine
New York, NY 10029
Dr. Jack Fowle
Reproductive Effects Assessment Group
U.S. Environmental Protection Agency
RD-689
Washi ngton, DC 20460
Dr. Bruce Fowler
Laboratory of Pharmacology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Or. Kristal Kostial
Institute for Medical Research
and Occupational Health
Yu-4100 Zagreb
Yugoslavia
Dr. Lawrence Kupper
Department of Biostatisties
UNC School of Public Health
Chapel Hill, NC 27514
Dr. Phillip Landrigan
Division of Surveillance,
Hazard Evaluation and Field Studies
Taft Laboratories - NIOSH
Cincinnati, OH 45226
Dr. David Lawrence
Microbiology and Immunology Dept.
Albany Medical College of Union
University
Albany, NY X220S
Dr. Jane Lin-Fu
Office of Maternal and Child Health
Department of Health and Human Services
Rockville, MO 20857
Dr. Don Lynam
Air Conservation
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. Ronald D. Hood
Department of Biology
The University of Alabama
University, AL 35486
Dr. V. Houk
Centers for Disease Control
1600 Clifton Road, NE
Atlanta, GA 30333
Dr. Loren D. Roller
School of Veterinary Medicine
University of Idaho
Moscow, ID 83843
Dr. Chuck Naumart
Exposure Assessment Group
U.S. Environmental Protection
Agency
Washington, DC 20460
Dr. Herbert L. Needleman
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Dr. H. Mitchell Perry
V.A. Medical Center
St. Louis, M0 63131
Dr. Jack Pierrard
E.I. duPont de Nemours and
Compancy, Inc.
Petroleum Laboratory
Wilmington, DE 19898
Dr. Sergio Piomelli
Columbia University Medical School
Division of Pediatric Hematology
and Oncology
New York, NY 10032
Or. Magnus Piscator
Department of Environmental Hygiene
The Karolinska Institute 104 01
Stockholm
Sweden
xxi
-------
Dr. Kathryn Mahaffey
Division of Nutrition
Food and Drug Administration
1090 Tusculum Avenue
Cincinnati, OH 45226
Dr. Ed McCabe
Department of Pediatrics
University of Wisconsin
Madison, WI 53706
Dr. Paul Mushak
Department of Pathology
UNC School of Medicine
Chapel Hill, NC 27514
Dr. John Rosen
Division of Pediatric Metabolism
Albert Einstein College of Medicine
Montefiore Hospital and Medical Center
111 East 210 Street
Bronx, NY 10467
Dr. Stephen R. Schroeder
Division for Disorders
of Development and Learning
Biological Sciences Research Center
University of North Carolina
Chapel Hill, NC 27514
Dr. Anna-Maria Seppalainen
Institutes of Occupational Health
Tyoterveyslaitos
Haartmaninkatu 1
00290 Helsinki 29
Finland
Dr. Ellen Silbergeld
Environmental Defense Fund
1525 18th Street, NW
Washington, DC 20036
Dr. Robert Putnam
International Lead-Z1nc
Research Organization
292 Madison Avenue
New York, NY 10017
Dr. Michael Rabinowitz
Children's Hospital Medical
Center
300 Longwood Avenue
Boston, MA 02115
Dr. Harry Roels
Unite de Toxicologic
Industrielle et Medicale
Universite de Louvain
Brussels, Belgium
Dr. Ron Snee
E.I. duPont Nemours and
Company, Inc.
Engineering Department L3167
Wilmington, DE 19898
Mr. Gary Ter Haar
Toxicology and Industrial
Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Mr. Ian von Lindern
Department of Chemical
Engineering
University of Idaho
Moscow, ID 83843
Dr. Richard P. Wedeen
V.A. Medical Center
Tremont Avenue
East Orange, NJ 07019
Chapter 8: Effects of Lead on Ecosystems
Principal Author
Dr. Robert Ellas
Environmental Criteria and Assessment Office
M0-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
xxii
-------
The following persons reviewed this chapter at EPA's request:
Dr. Clarence A. Hall
Air Conservation Division
Ethyl Corporation
1600 West 8-Mile Road
Ferndale, MI 48220
Dr. Gary Rolfe
Department of Forestry
University of Illinois
Urbana, IL 61801
Or. Derek Hodgson
Department of Chemsitry
University of North Carolina
Chapel Hill, NC 27514
Dr. Glen Sanderson
Illinois Natural History Survey
University of Illinois
Urbana, IL 61801
Dr. David E. Koeppe
Department of Plant and Soil Science
P.O. Box 4169
Texas Technical University
Lubbock, TX 79409
Dr. Samuel Lestz
Department of Mechanical Engineering
Pennsylvania State University
University Park, PA 16802
Dr. Ben Y. H. Liu
Department of Mechanical Engineering
University of Minnesota
Minneapolis, MN 55455
Or. Rodney K. Skogerboe
Department of Chemistry
Colorado State University
Fort Collins, CO 80521
Dr. William H. Smith
Greeley Memorial Laboratory
and Environmental Studies
Yale University, School of
Forestry
New Haven, CT 06511
Dr. Gary Ter Haar
Toxicology and Industrial Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. Michael Oppenheimer
Environmental Oefense Fund
444 Park Avenue, S.
New York, NY 10016
Dr. James Wedding
Engineering Research Center
Colorado State University
Fort Collins, CO 80523
Dr. William Pierson
Scientific Research Labs.
Ford Motor Company
P.O. Box 2053
Dearborn, MI 48121
XX i i i
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-------
PRELIMINARY DRAFT
2. INTRODUCTION
According to Section 108 of the Clean Air Act of 1970, as amended in June 1974, a cri-
teria document for a specific pollutant or class of pollutants shall
. . . accurately reflect the latest scientific knowledge useful in
indicating the kind and extent of all identifiable effects on public
health or welfare which may be expected from the presence of such pollu-
tant in the ambient air, in varying quantities.
Air quality criteria are of necessity based on presently available scientific data, which
in turn reflect the sophistication of the technology used in obtaining those data as well as
the magnitude of the experimental efforts expended. Thus air quality criteria for atmospheric
pollutants are a scientific expression of current knowledge and uncertainties. Specifically,
air quality criteria are expressions of the scientific knowledge of the relationships between
various concentrations—averaged over a suitable time period—of pollutants in the same atmos-
phere and their adverse effects upon public health and the environment. Criteria are issued
to help make decisions about the need for control of a pollutant and about the development of
air quality standards governing the pollutant. Air quality criteria are descriptive: that
is, they describe the effects that have been observed to occur as a result of external expo-
sure at specific levels of a pollutant. In contrast, air quality standards are prescriptive:
that is, they prescribe what a political jurisdiction has determined to be the maximum per-
missible exposure for a given time in a specified geographic area.
In the case of criteria for pollutants that appear in the atmosphere only in the gas
phase (and thus remain airborne), the sources, levels, and effects of exposure must be con-
sidered only as they affect the human population through inhalation of or external contact
with that pollutant. Lead, however, is found 1n the atmosphere primarily as Inorganic partic-
ulate, with only a small fraction normally occurring as vapor-phase organic lead. Conse-
quently, inhalation and contact are but two of the routes by which human populations may be
exposed to lead. Some particulate lead may remain suspended in the air and enter the human
bo4y only by inhalation, but other lead-containing particles will be deposited on vegetation,
surface waters, dust, soil, pavements, interior and exterior surfaces of hous1ng--in fact, on
any surface in contact with the air. Thus criteria for lead must be developed that will take
Into account all principal routes of exposure of the human population.
This criteria document 1s a revision of the previous Air Quality Criteria Document for
Lead (EPA-600/8-77-017) published in December, 1977. This revision 1s mandated by the Clean
Air Act (Sect. 108 and 109), as amended U.S.C. §§7408 and 7409. The criteria document sets
forth what is known about the effects of lead contamination In the environment on human
health and welfare. This requires that the relationship between levels of exposure to lead,
D23PB2
2-1
7/1/83
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PRELIMINARY DRAFT
via all routes and averaged over a suitable time period, and the biological responses to those
levels be carefully assessed. Assessment of exposure must take into consideration the
temporal and spatial distribution of lead and its various forms In the environment.
This document focuses primarily on lead as found in its various forms in the ambient
atmosphere; in order to assess its effects on human health, however, the distribution and
biological availability of lead in other environmental media have been considered. The
rationale for structuring the document was based primarily on the two major questions of
exposure and response. The first portion of the document is devoted to lead in the environ-
ment—its physical and chemical properties; the monitoring of lead in various media;
sources, emissions, and concentrations of lead; and the transport and transformation of lead
within environmental media. The later chapters are devoted to discussion of biological
responses and effects on ecosystems and human health.
In order to facilitate printing, distribution, and review of the present draft materials,
this First External Review Draft of the revised EPA Air Quality Criteria Document for Lead
is being released in the form of four volumes. The first volume (Volume I) contains the
executive summary and conclusions chapter (Chapter 1) for the entire document. Volume II (the
present volume) contains Chapters 2-8, which include: the introduction for the document
(Chapter 2); discussions of the above listed topics concerning lead in the environment
(Chapters 3-7); and evaluation of lead effects on ecosystems (Chapter 8). The remaining two
volumes contain Chapters 9-13, which deal with the extensive available literature relevant to
assessment of health effects associated with lead exposure.
An effort has been made to limit the document to a highly critical assessment of the
scientific data base. The scientific literature has been reviewed through June 1983. The
references cited do not constitute an exhaustive bibliography of all available lead-related
literature but they are thought to be sufficient to reflect the current state of knowledge on
those issues most relevant to the review of the air quality standard for lead.
The status of control technology for lead is not discussed 1n this document. For infor-
mation on the subject, the reader Is referred to appropriate control technology documentation
published by the Office of Air Quality Planning and Standards (OAQPS), EPA. The subject of
adequate margin of safety stipulated in Section 108 of the Clean Air Act also is not explicity
addressed here; this topic will be considered in depth by EPA's Office of Air Quality Planning
and Standards in documentation prepared as a part of the process of revising the National
Ambient Air Quality Standard for Lead.
D23PB2
2-2
7/1/83
-------
PRELIMINARY DRAFT
3. CHEMICAL AND PHYSICAL PROPERTIES
3.1 INTRODUCTION
Lead is a gray-white metal of bright luster that, because of its easy isolation and low
melting point (327.5°C), was among the first of the metals to be placed in the service of roan.
Lead was used as early as 2000 B.C. by the Phoenicians, who traveled as far as Spain and
England to mine it, and it was used extensively by the Egyptians; the British Museum contains
a lead figure found in an Egyptian temple which possibly dates from 3000 B.C. The most
abundant ore is galena, in which lead is present as the sulfide (PbS), and from which metallic
lead is readily smelted. The metal 1s soft, malleable, and ductile, a poor electrical
conductor, and highly impervious to corrosion. This unique combination of physical properties
has led to its use in piping and roofing, and in containers for corrosive liquids. By the
time of the Roman Empire, it was already in wide use in aqueducts and public water systems, as
well as in cooking and storage utensils. Its alloys are used as solder, type metal, and
various antifriction materials. The metal and the dioxide are used in storage batteries, and
much metal is used in cable covering, plumbing and ammunition. Because of its high nuclear
cross section, lead is extensively used-as a radiation shield around X-ray equipment and
nuclear reactors.
3.2 ELEMENTAL LEAD
In comparison with the most abundant metals in the earth's crust (aluminum and iron),
lead is a rare metal; even copper and zinc are more abundant by factors of five and eight,
respectively. Lead is, however, more abundant than the other toxic heavy metals; its
abundance in the earth's crust has been estimated (Moeller, 1952) to be as high as 1.6 x 10 3
percent, although some other authors (Heslop and Jones, 1976) suggest a lower value of 2 x
10 4 percent. Either of these estimates suggests that the abundance of lead is more than 100
times that of cadmium or mercury, two other significant systemic metallic poisons. More
important, since lead occurs in highly concentrated ores from which it is readily separated,
the availability of lead 1s far greater than its natural abundance would suggest. The great
environmental significance of lead is the result both of its utility and of Its availability.
Lead ranks fifth among metals in tonnage consumed, after iron, copper, aluminum and zinc; it
is, therefore, produced in far larger quantities than any other toxic heavy metal (Dyrssen,
1972). The properties of elemental lead are summarized in Table 3-1.
023PB3/A
3-1
7/13/83
-------
PRELIMINARY DRAFT
TABLE 3-1. PROPERTIES OF ELEMENTAL LEAD
Property
Description
Atonic weight
Atonic number
Oxidation states
Density
Melting point
Boiling point
Covalent radius (tetradehral)
Ionic radii
Resistivity
207.19
82
+2, +4
11.35 g/cm3 at 20 °C
327.5 °C
1740 °C
1.44 A
1.21 A (+2), 0.78 A (+4)
21.9 x 10~6 ohm/cm
Natural lead is a Mixture of four stable isotopes: 204Pb (VL.5 percent), 20®Pb (23.6
percent), 207Pb (22.6 percent), and 208Pb (52.3 percent). There is no radioactive progenitor
for 204Pb, but 208Pb, 207Pb, and 208Pb are produced by the radioactive decay of 238U, 28BU,
and 232Th, respectively. There are four radioactive isotopes of lead that occur as members of
these decay series. Of these, only 210Pb is long lived, with a half-life of 22 years. The
others are 211Pb (half-life 36.1 m1n), 212Pb (10.64 hr), and 214Pb (26.8 min). The stable
isotopic compositions of naturally occurring lead ores are not identical, but show variations
reflecting geological evolution (Russell and Farquhar, 1960). Thus, the observed isotopic
ratios depend upon the U/Pb and Th/Pb ratios of the source from which the ore is derived and
the age of the ore deposit. The 208Pb/204Pb Isotopic ratio, for example, varies from
approximately 16.5 to 21 depending on the source (Doe, 1970). The isotopic ratios in average
crustal rock reflect the continuing decay of uranium and thorium. The differences between
crustal rock and ore bodies, and between major ore bodies in various parts of the world, often
permit the identification of the source of lead in the environment.
3.3 GENERAL CHEMISTRY OF LEAD
Lead is the heaviest element In Group IVB of the periodic table; this is the group that
also contains carbon, silicon, germanium, and tin. Unlike the chemistry of carbon, however,
the inorganic chemistry of lead is dominated by the divalent (+2) oxidation state rather than
023PB3/A 3-2 7/13/83
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PRELIMINARY DRAFT
the tetravalent (+4) oxidation state. This Important chemical feature is a direct result; of
the fact that the strengths of single bonds between the Group IV atoms and other atoms
generally decrease as the atomic number of the Group IV atom increases (Cotton and Wilkinson,
1980). Thus, the average energy of a C-H bond is 100 kcal/mole, and it is this factor that
stabilizes CH4 relative to CH2; for lead, the Pb-H energy is only approximately 50 kcal/mole
(Shaw and All red, 1970), and this is presumably too small to compensate for the Pb(II) ¦*
Pb(IV) promotional energy. It is this Same feature that explains the marked difference in the
tendencies to catenation shown by these elements. Though C-C bonds are present in literally
millions of compounds, for lead catenation occurs only in organolead compounds. Lead does,
however, form compounds like Na4Pb9 which contain distinct polyatomic lead clusters (Britton,
1964), and Pb-Pb bonds are found in the cationlc cluster [Pba0(0H)e]+4 (Olin and Soderqulst,
1972).
A listing of the solubilities and physical properties of the more common compounds of
lead is given in Appendix 3A. As can be discerned from those data, most Inorganic lead salts
are sparingly soluble (e.g., PbF2, PbCl2) or virtually insoluble (PbS04, PbCr04) in water; the
notable exceptions are lead nitrate, Pb(N03)2, and lead acetate, Pb(0C0CHs)2. Inorganic lead
(II) salts are, for the most part, relatively high-melting-point solids with correspondingly
low vapor pressures at room temperatures. The vapor pressures of the most commonly
encountered lead salts are also tabulated in Appendix 3A. The transformation of lead salts In
the atmosphere is discussed in Chapter i.
3.4 0RGAN0METALLIC CHEMISTRY OF LEAD
The properties of organolead compounds (I.e., compounds containing bonds between lead and
carbon) are entirely different from those of the inorganic compounds of lead; although a few
organolead(II) compounds, such as dicyclopentadienyllead, Pb(C5Hs)2, are known, the organic
chemistry of lead is dominated by the tetravalent (+4) oxidation state. An important property
of most organolead compounds is that they undergo photolysis when exposed to light (Rufman and
Rotenberg, 1980).
Because of their use as antiknock agents in gasoline and other fuels, the most Important
organolead compounds have been the tetraalkyl compounds tetraethyllead (TEL) and
tetramethyHead (TML). As would be expected for such nonpolar compounds, TEL and TML are
Insoluble in water but soluble in hydrocarbon solvents (e.g., gasoline). These two compounds
are manufactured by the reaction of the alkyl chloride with lead-sodium alloy (Shapiro and
Frey, 1968):
4NaPb + 4CaHBCl (C8H6)4Pb ~ 3Pb + 4NaCl (3-1)
023PB3/A
3-3
7/13/83
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PRELIMINARY DRAFT
The methyl compound, TML, is also manufactured by a Grignard process involving the
electrolysis of lead pellets in methylmagnesium chloride (Shapiro and Frey, 1968):
A common type of commercial antiknock mixture contains a chemically redistributed mixture
of alky "Head compounds. In the presence of Lewis acid catalysts, a mixture of TEL and TML
undergoes a redistribution reaction to produce an equilibrium mixture of the five possible
tetraalkyllead compounds. For example, an equimolar mixture of TEL and TML produces a product
with a composition as shown below:
These lead compounds are removed from internal combustion engines by a process called
lead scavenging, in which they react in the combustion chamber with halogenated hydrocarbon
additives (notably ethylene dibromide and ethylene dichloride) to form lead halides, usually
bromochlorolead(II). Mobile source emissions are discussed in detail in Section 5.3.3.2.
Several hundred other organolead compounds have been synthesized, and the properties of
many of them are reported by Shapiro and Frey (1968). The continuing importance of organolead
chemistry is demonstrated by a variety of recent publications investigating the syntheses
(Hager and Huber, 1980, Wharf et al., 1980) and structures (Barkigia, et al., 1980) of
organolead complexes, and by recent patents for lead catalysts (Nishikido, et al., 1980).
3.5 FORMATION OF CHELATES AND OTHER COMPLEXES
The bonding in organometallic derivatives of lead is principally covalent rather than
Ionic because of the small difference in the electronegativities of lead (1.8) and carbon
(2.6). As is the case in virtually all metal complexes, however, the bonding is of the
donor-acceptor type, in which both electrons in the bonding orbital originate from the carbon
atom.
The donor atoms in a metal complex could be almost any basic atom or molecule; the only
requirement is that a donor, usually called a 1igand, must have a pair of electrons available
2CH3MgCl + 2CHaCl + Pb -» (CH3)«Pb + 2MgCl2
(3-2)
Component
(CH8)4Pb
MoT percent
4.6
24.8
41.2
24.8
4.6
(CH3)3Pb(C2Hs)
(CH3)2Pb(C2H5)2
(CH3)Pb(C2H6)3
(C2Hs)4Pb
023PB3/A
3-4
7/13/83
-------
PRELIMINARY DRAFT
for bond formation. In general, the metal atom occupies a central position in the complex, as
exemplified by the lead atom in tetramethyl1ead (Figure 3-la) which is tetrahedrally
surrounded by four methyl groups. In these simple organolead compounds, the lead is usually
present as Pb(IV), and the complexes are relatively inert. These simple ligands, which bind
to metal at only a single site, are called monodentate ligands. Some ligands, however, can
bind to the metal atom by more than one donor atom, so as to form a heterocyclic ring
structure. Rings of this general type are called chelate rings, and the donor molecules which
form them are called polydentate ligands or chelating agents. In the chemistry of lead,
chelation normally involves Pb(II), leading to kinetically quite labile (although
thermodynamically stable) octahedral complexes. A wide variety of biologically significant
chelates with ligands, such as amino acids, peptides, nucleotides and similar macromolecules,
are known. The simplest structure of this type occurs with the amino acid glycine, as
represented in Figure 3-lb for a 1:2 (metal:1igand) complex. The importance of chelating
agents in the present context is their widespread use in the treatment of lead and other metal
poisoning.
Metals are often classified according to some combination of their electronegativity,
ionic radius and formal charge (Ahrland, 1966, 1968, 1973; Basolo and Pearson, 1967; Nleboer
and Richardson, 1980; Pearson, 1963, 1968). These parameters are used to construct empirical
classification schemes of relative hardness or softness. In these schemes, "hard" metals form
strong bonds with "hard" anions and likewise "soft" metals with "soft" anions. Some metals
are borderline, having both soft and hard character. Pb(II), although borderline,
demonstrates primarily soft character (Figure 3-2). The terms Class A may also be used to
refer to hard metals, and Class 8 to soft metals. Since Pb(II) is a relatively soft (or class
B) metal ion, it forms strong bonds to soft donor atoms like the sulfur atoms in the cysteine
residues of proteins and enzymes; it also coordinates strongly with the imidazole groups of
histidine residues and with the carboxyl groups of glutamic and aspartlc acid residues. In
living systems, therefore, lead atoms bind to these peptide residues in proteins, thereby
preventing the proteins from carrying out their functions by changing the tertiary structure
of the protein or by blocking the substrate's approach to the active site of the protein. As
has been demonstrated fn several studies (Jones and Vaughn, 1978; Williams and Turner, 1981;
Williams et al. , 1982), there is an Inverse correlation between the LD50 values of metal
complexes and the chemical softness parameter (op) (Pearson and Mawby, 1967). Thus, for both
mice and Drosophila. soft metal ions like lead(II) have been found to be more toxic than hard
metal ions (Williams et al., 1982). This classification of metal ions according to their
toxicity has been discussed in detail by Nieboer and Richardson (1980). Lead(II) has a higher
softness parameter than either cadmiun(II) or mercury(II), so lead(II) compounds would not be
expected to be as toxic as their cadmium or mercury analogues.
023PB3/A 3-5 7/13/83
-------
PRELIMINARY ORAFT
023PB3/A
H3c CH3
V
H3(^ CH3
(a)
9.0
£
X
£ 3.0
iu
5 26
8 "
ec
O 2.0
CO
8 15
5 "
O
1.0
0.6
0
>
4.6
—
• Aa*
4.0
"Iti*
3.6
—»Cu-
Au*
Figure 3-1. Metal complexes of lead.
i—i—i—i—i—r~i—rTT
,
Pd**
Ha*
e T1"
PMIV) —J
CLASS B _
• Pt>»*
- ^ *""• ecu-
cd-e
Crj!
W&MZn"
Mn"» V*
In"
eswiiu
Asfllll
• F«"
Qa**e
Sn(IV) •
BORDERLINE
Mg"
C»" Bt" •
\K' C»'-
>Na* 8r»*
— U'
Qd'
Lu»-
• ••# #
Sc*
La1-
Y**
Al"
Be'"
J I I L
CLASS A
J 1 1 // I //J-
4 6 8 10 12 14 16 20 23
CLASS A OR IONIC INDEX, Z*/r
Figure 3-2. Softness parameters of metals.
Source: Nieboer and Richardson (1980).
3-6
7/01/83
-------
PRELIMINARY DRAFT
O
It
/
N-CH2-CH2-N
\
/
ch2-c-o
ch3 nh2 oh
CH2-C-0-
II
EDTA
PENICILLAMINE
Rgure 3-3. Structure of chelating agents.
The role of the chelating agents 1s to compete with the peptides for the metal by forming
stable chelate complexes that can be transported froa the protein and eventually be exreted by
the body. For simple thermodynamic reasons (see Appendix 3A), chelate complexes are much more
stable than inonodentate aetal complexes, and it is this enhanced stability that is the basis
for their ability to compete favorably with proteins and other ligands for the metal ions.
The chelating agents most commonly used for the treatment of lead poisoning are ethylenediami-
netetraacetate ions (EDTA), 0-penici11 amine (Figure 3-3) and their derivatives. EDTA is known
to act as a hexadentate ligand toward metals (Lis, 1978; McCandlish et al., 1978). X-ray
diffraction studies have demonstrated that D-penicillamine is a tridentate ligand binding
through its sulfur, nitrogen and oxygen atoms to cobalt (de Meester and Hodgson, 1977a; Hells;
et al., 1977), chromium (de Meester and Hodgson, 1977b), cadmium (Freeman et al., 1976), and
lead itself (Freeman et al., 1974), but both penicillamine and other cysteine derivatives may
act as bidentate ligands (Carty and Taylor, 1977; de Meester and Hodgson, 1977c). Moreover,
penicillamine binds to mercury only through its sulfur atoms (Wong et al., 1973; Carty and
Taylor, 1976).
It should be noted that both the stoichiometry and structures of metal chelates depend
upon pH, and that structures different from those manifest in solution may occur in crystals.
It will suffice to state, however, that several ligands can be found that are capable of suffi
ciently strong chelation with lead present in the body under physiological conditions to per-
mit their use in the effective treatment of lead poisoning.
023PB3/A 3-7 7/01/83
-------
PRELIMINARY DftAFT
3.6 REFERENCES
Ahrland, S. (1966) Factors contributing to (b)-behaviour in acceptors. Struct. Bonding I: 207-
220.
Ahrland, S. (1968) Thermodynamics of complex formation between hard and soft acceptors and
donors. Struct. Bonding (Berlin) 5: 118-149.
Ahrland, S. (1973) Thermodynamics of the stepwise formation of metal-ion complexes in aqueous
solution. Struct. Bonding (Berlin) 15: 167-188.
Barkigia, K. M.; Fajer, J.; Adler, A. D.; Williams, 6. J. B. (1980) Crystal and molecular struc-
ture of (5,l0,l5,20-tetra-n-propylporph1nato)lead(II): a "roof" porphyrin. Inorg. Chew.
19: 2057-2061.
Basolo, F.; Pearson, R. G. (1967) Mechanisms of inorganic reactions: a study of metal complexes
in solution. New York, NY: John Wiley & Sons, Inc.; pp. 23-25, 113-119.
Britton, D. (1964) The structure of the Pb^ 4 ion. Inorg. Chem. 3: 305.
Carty, A. J.; Taylor, N. J. (1976) Binding of inorganic mercury at biological sites. J. Chem.
Soc. Chem. Commun. (6): 214-216.
Carty, A. J.; Taylor, N. J. (1977) Binding of heavy metals at biologically important sites:
synthesis and molecular structure of aquo(bromo)-DL-penicil1aminatocadmium(II) d1hydrate.
Inorg. Chem. 16: 177-181.
Cotton, F. A.; Wilkinson, G. (1980) Advanced inorganic chemistry. New York, NY: John Wiley &
Sons, Inc.
d# Meester, P.; Hodgson, 0. J. (1977a) Model for the binding of D-penicillamine to metal ions
in living systems: synthesis and structure of L-histidinyl-D-penicillaminatocobalt(in)
monohydrate, [Co(L-his)(D-pen)] H20. J. Am. Chem. Soc. 99: 101-104.
de Meester, P.; Hodgson, D. J. (1977b) Synthesis and structural characterization of L-
hist1d1nato-D-penicil1am1natochro»ium (III) monohydrate, J. Chem. Soc. Oalton Trans. (17):
1604-1607. ~
de Meester, P.; Hodgson, "0. J. (1977c) Absence of metal interaction with sulfur in two metal
complexes of a cysteine derivative: the structural characterization of Bis(S-nethyl-L-
cysteinato)cadmlum(II) and Bis(S-methy1-L-cyste1nato)zinc(II). J. Am. Chem. Soc. 99: 6884-
6889*
Doe, B. R. (1970) Lead isotopes. New York, NY: Sprlnger-Verlag. (Engelhardt, W.; Hahn, T.; Roy,
R.; Winchester, J. W.; Wyllie, P. J., eds. Minerals, rocks and inorganic materials:
monograph series of theoretical and experimental studies: v. 3).
Oyrssen, D. (1972) The changing chemistry of the oceans. Ambio 1: 21-25.
Freeman, H. C.; Stevens, G. N.; Taylor, I. F., Jr. (1974) Metal binding in chelation therapy:
the crystal structure of D-penicillaminatolead(II). J. Chem. Soc. Chem. Commun. (10):
366-367.
Freeman, H. C. ; Huq, F.; Stevens, G. N. (1976) Metal binding by 0-penlcillamine: crystal struc-
ture of D*penici11 aminatocadmium(11) hydrate. J. Chem. Soc. Chem. Commun. (3): 90-91.
A03REF/A 3-8 7/13/83
-------
PRELIMINARY DRAFT
Freeman, H. C.; Huq, F.; Stevens, G. N. (1976) Metal binding by D-penicillamine: crystal struc-
ture of D-peni ci 17ami natocadmi um( 11) hydrate. J. Chem. Soc. Chew. Commun. (3): 90-91.
Hager, C-D.; Huber, F. (1980) Organobleiverbindungen won MercaptocarbonsSuren. [Organolead com-
pounds of mercaptocarboxylic acids.] Z. Naturforsch. 35b: S42-547.
Hells, H. M.; de Meester, P.; Hodgson, D. J. (1977) Binding of penicillamine to toxic metal
ions: synthesis and structure of potassium(D-pen1c1llam1nato) (L-Penicniamlnato)cobal-
tate(III) dihydrate, K[Co(D-pen)(l-pen)] 2H20. J. Am. Chem. Soc. 99: 3309-3312.
Heslop, R. B.; Jones, K. (1976) Inorganic chemistry: a guide to advanced study. New York, NY:
Elsevier Science Publishing Co.; pp. 402-403.
Jones, M. M.; Vaughn, W. K. (1978) HSA6 theory and acute metal ion toxicity and detoxification
processes. J. Inorg. Nucl. Chem. 40: 2081-2088.
Lis, T. (1978) Potassium ethylenedianHnetetraacetatomanganate(III) dihydrate. Acta Crystallogr.
Sec. 8 34: 1342-1344.
McCandlish, E. F. K.; Michael, T. K.; Neal, J. A.; Lingafelter, E. C.; Rose, N. J. (1978) Com-
parison of the structures and aqueous solutions of [o-phenylened1am1netetraacetato(4-)]
cobalt(II) and [ethylenediaminetetraacetato(4-)] cobaft(II) ions. Inorg. Chem. 17: 1383-
1394.
Moeller, T. (1952) Inorganic chemistry: an advanced textbook. New York, NY: John Wiley & Sons,
Inc.
Nieboer, E.; Richardson, 0. H. S. (1980) The replacement of the nondescript term "heavy metals"
by a biologically and chemically significant classification of metal ions. Environ.
Pollut. Ser. B. 1: 3-26.
Nishikido, J.; Tamura, N.; Fukuoka, Y. (1980) (Asahi Chemical Industry Co. Ltd.) Ger. Patent
No. 2,936,652.
011 n, A.; SSderquist, R. (1972) The crystal structure of p-[PbeO(0H)6](C104)4 H20. Acta Chem.
Scand. 26: 3505-3514.
Pearson, R. G. (1963) Hard and soft acids and bases. J. Am. Chem. Soc. 85: 3533-3539.
Pearson, R. G. (1968) Hard and soft acids and bases, HSAB, part 1: fundamental principles. J.
Chem. Educ. 45: 581-587.
Pearson, R. G.; Mawby, R. J. (1967) The nature of metal-halogen bonds. In: Gutmann, V., ed.
Halogen chemistry: vol. 3. New York, NY: Academic Press, Inc.; pp. 55-84.
Rufman, N. M.; Rotenberg, Z. A. (1980) Special kinetic features of the photodecomposition of
organolead compounds at lead electrode surfaces. Sov. Electrochem. Engl. Transl. 16:
309-314.
Russell, R.; Farquhar, R. (1960) Introduction. In: Lead Isotopes in geology. New York, NY:
Interscience; pp. 1-12.
Shapiro, H.; Frey, F. W. (1968) The organic compounds of lead. New York, NY: John Wiley & Sons.
(Seyferth, 0., ed. The chemistry of organometalllc compounds: a series of monographs.)
03REF
3-9
7/1/83
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PRELIMINARY DRAFT
Shaw, C. F., III; Allred, A. L. (1970) Nonbonded Interactions in organometallic compounds of
Group IV B. Organometallic Chem. Rev. A 5: 95-142.
Wharf, I.; Onyszchuk, M.; Miller, J. M.; Jones, T. R. B. (1980) Synthesis and spectroscopic
studies of phenyl lead hallde and thlocyanate adducts with hexamethylphosphoramide. J.
Organonet. Chem. 190: 417-433.
Williams, M. W.; Hoeschele, J. D.; Turner, J. E.; Jacobson, K. B.; Christie, N. T.; Paton,
C. L.; Smith, L. H.; Witsch, H. R.; Lee, E. H. (1982) Chemical softness and acute metal
toxicity 1n mice and Drosophila. Toxicol. Appl. Pharmacol. 63: 461-469.
Williams, M. W.; Turner, J. E. (1981) Comments on softness parameters and metal ion toxicity.
J. Inorg. Nucl. Chem. 43: 1689-1691.
Wong, Y. S.; Chieh, P. C.; Carty, A. J. (1973) Binding of methylmercury by anino-aclds: X-ray
structures of D.L-penici11 aminatomethv1mercurvf11)¦ J. Chem. Soc. Chem. Commun. (19):
741-742.
03REF
3-10
7/1/83
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PRELIMINARY DRAFT
APPENDIX 3A
PHYSICAL/CHEMICAL OATA FOR LEAD COMPOUNDS
3A.1 DATA TABLES
Table 3A*1. PHYSICAL PROPERTIES OF INORGANIC LEAD COMPOUNDS1
Solubility, g/100 ml
Conpourtd
Formula
M.W.
S.G.
M.P.
Cold
water
Hot
water
Other
solvents
Lead
Pb
207.19
11.35
327.5
i
1
sa
Acetate
Pb{CaH302)2
325.28
3.25
280
44.3
22l«o
s glyc
Azlde
Pb(Ns)2
291.23
-
expl.
0.023
0.0970
.
Bromate
Pb(Br03)2*H20
481.02
5.53
dl80
1.38
si s
-
Bro»ide
PbBrs
367.01
6.66
373
0.8441
4.71100
sa
Carbonate
PbC03
267.20
6.6
d315
0.00011
d
sa.alk
Carbonate,
basic
2PbC03-Pb(0H)2
775.60
6.14
d400
i
i
s HN03
Chloride
PbCl2
278.10
5.85
501
0.99
3.34100
1 al
Chlorobromlde
PbClBr
322.56
Chroawte
PbCr04
323.18
6.12
844
6x10*
1
sa.alk
Chronate,
basic
PbCr04-Pb0
546.37
6.63
1
1
sa,alk
Cyanide
Pb(CN)2
259-23
si s
s
s KCN
Fluoride
PbF2
245.19
8.24
855
0.064
S HNOa
FluorochloHde
PbFCl
261.64
7.05
601
0.037
0.1081
Fomate
Pb(CH02)2
297.23
4.63
dl90
1.6
20
i al
Hydride
PbH2
209.21
d
Hydroxide
Pb(OH)2
241.20
dl45
0.0155
si s
sa.alk
Iodate
Pb{103)2
557.00
6.155 d300
0.0012
0.003
s HN08
Iodide
Pbl2
461.00
6.16
402
0.063
0.41
s,a1k
Nitrate
Pb(N03)2
331.20
4.53
d470
37.65
127
s.alk
PBAPP/A
3A-1
7/1/83
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PRELIMINARY DRAFT
Table 3A-1. (continued). PHYSICAL PROPERTIES OF INORGANIC LEAD COMPOUNDS1
Solubility, q/100 ml
Cold Hot Other
Compound
Formula
M.W.
S.G.
M.P.
water
water solvents
Nitrate, basic
Pb(0H)N03
286.20
5.93
dl80
19.4
s
sa
Oxalate
PbC204
295.21
5.28
d300
0.00016
sa
Oxide
PbO
223.19
9.53
888
0.0017
s,alk
Dioxide
Pb02
239.19
9.375
d290
i
i
sa
Oxide (red)
Pb304
685.57
9.1
d500
i
i
sa
Phosphate
Pb3(P04)2
811.51
7
1014
1.4x10" 8
1
s.alk
Sulfate
PbS04
303.25
6.2
1170
0.00425
0.0056
Sulfide
PbS
239.25
7.5
1114
8.6x10s
sa
Sulfite
PbS03
287.25
d
i
i
sa
Thiocyanate
Pb(SCN)2
323.35
3.82
dl90
0.05
0.2
s.alk
Abbreviations: a - acid; al - alcohol; alk - alkali; d - decomposes;
expl - explodes; glyc - glycol; i - insoluble; s - soluble;
M.W. - molecular weight; S.6. - specific gravity; and
M.P. - i»elting point.
Source: Weast, 1975.
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Table 3A-2. TEMPERATURE VARIATION OF THE VAPOR PRESSURES
OF COMMON LEAD COMPOUNDS
Temperature °C
Name
Formula
M.P.
1 mm
10 Ml
40 mm
100 mm
400 mm
760 mm
Lead
Pb
327.4
973
1162
1309
1421
1630
1744
Lead
bromide
PbBr2
373
513
610
686
745
856
914
Lead
chloride
PbCl2
501
547
648
725
784
893
954
Lead
flourlde
PbF2
855
solid
904
1003
1080
1219
1293
Lead
iodide
Pbl2
402
479
571
644
701
807
872
Lead
oxide
PbO
890
943
1085
1189
1265
1402
1472
Lead
sulfide
PbS
1114
852
975
1048
1108
1221
1281
(solid)
(solid)
(solid)
(solid)
Source: Stull, 1947
3A.2. THE CHELATE EFFECT
The stability constants of chelated complexes are normally several orders of magnitude
higher than those of comparable monodentate complexes; this effect is called the chelate
effect, and is very readily explained In terns of kinetic considerations. A comparison of the
binding of a single bidentate 1igand with that of two molecules of a chemically similar mono-
dentate 11gand shows that, for the monodentate case, the process can be represented by the
equations:
M ~ B *a M-B (3A_1)
M-B + B
kc MB2 (3A-2)
kd
The related expressions for the bidentate case are:
M ~ B-B M-B-B (3A-3)
*2
k3 |j B (3A-4)
M-B-B k< B
The overall equilibrium constants, therefore, are:
Ki - Vk.
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PRELIMINARY DRAFT
For a given metal, M, and two ligands, B and B-B, which are chemically similar, It 1s
established that kt and have similar values to each other, as do k2 and k^ and k< and kd;
each of these pairs of terms represents chemically similar processes. The origin of the
chelate effect Has in the very large value of k3 relative to that of kc- This comes about
because k3 represents a unimolecular process, whereas kc is a bimolecular rate constant.
Consequently, K2 » Kt.
This concept can, of course, be extended to polydentate llgands; in general, the more
extensive the chelation, the no re stable the netal complex. Hence, one would anticipate,
correctly, that polydentate chelating agents such as penicillamine or EDTA can form extremely
stable complexes with metal ions.
3A.3 REFERENCES
Stull, D.R. (1947) Vapor pressure of pure substances; organic compounds. Ind. Eng. Chen 39;
517-540.
Weast, R.C., ed. (1975) Handbook of chemistry and physics. Cleveland, OH; The Chemical Rubber
Co.
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4. SAMPLING AND ANALYTICAL METHODS FOR ENVIRONMENTAL LEAD
4.1 INTRODUCTION
Lead, like all criteria pollutants, has a designated Reference Method for monitoring and
analysis as required in State Implementation Plans for determining compliance with the lead
National Ambient Air Quality Standard. The Reference Method [C.F.R. (1982) 40;§80] uses a
high volume sampler
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PRELIMINARY DRAFT
4.2 SAMPLING
The purpose of sampling is to determine the nature and concentration of lead in the envi-
ronment. Sampling strategy is dictated by research needs. This strategy encompasses site
selection, choice of instrument used to obtain representative samples, and choice of method
used to preserve sample integrity. In the United States, sampling stations for air pollutants
have been operated since the early 1950's. These early stations were a part of the National
Air Surveillance Network (NASN), which has now become the National Filter Analysis Network
(NFAN). Two other types of networks have been established to meet specific data requirements.
State and Local Air Monitoring Stations (SLAMS) provide data from specific areas where pollu-
tant concentrations and population densities are the greatest and where monitoring of compli-
ance to standards is critical. The National Air Monitoring Station (NAMS) network is designed
to serve national monitoring needs, including assessment of national ambient trends. SLAMS
and NAMS stations are maintained by state and local agencies and the air samples are analyzed
in their laboratories. Stations in the NFAN network are maintained by state and local agen-
cies, but the samples are analyzed by laboratories in the U.S. Environmental Protection
Agency, where quality control procedures are rigorously maintained.
Data from all three networks are combined into one data base, the National Aerometric
Data Bank (NADfi). These data may be individual chemical analyses of a 24-hour sampling period
arithmetically averaged over a calendar period, or chemical composites of several filters used
to determine a quarterly composite. Data are occasionally not available because they do not
conform to strict statistical requirements. A summary of the data from the NADB appears in
Section 7.2.1.
4.2.1 Regulatory Siting Criteria for Ambient Aerosol Samplers
In September of 1981, EPA promulgated regulations establishing ambient air monitoring and
data reporting requirements for lead [C.F.R, (1982) 40:§58] comparable to those already estab-
lished in May of 1979 for the other criteria pollutants. Whereas sampling for lead is accomp-
lished when sampling for TSP, the designs of lead and TSP monitoring stations must be comple-
mentary to insure compliance with the NAMS criteria for each pollutant, as presented in Table
4-1, Table 4-2, and Figure 4-1.
In general, the criteria with respect to monitoring stations designate that there must be
at least two SLAMS sites for lead in any area which has a population greater than 500,000 and/
or any area where lead concentration currently exceeds the ambient lead standard (1.5 jjg/m3)
or has exceeded it since January 1, 1974. In such areas, the SLAMS sites designated as part
of the NAMS network must include a microscale or middlescale site located near a major roadway
(230,000 ADT), as well as a neighborhood scale site located in a highly populated residential
sector with high traffic density (430,000 ADT).
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TABLE 4-1. DESIGN OF NATIONAL AIR MONITORING STATIONS
Criteria
TSP (Final Rule)
Air Pb (Final Rule)
Spatial scale
Category (a)
Category (b)
Number required
Category (a)
Meters from edge of
roadway
meters above ground
level
Category (b)
Meters from edge of
Meters above ground
Stations required
Neighborhood scale
As per Table 4-2
Siting
High traffic and
population density
neighborhood scale
—>3000
As per Figure 4-1
2-15
roadway
level
Microscale or middle scale
Neighborhood scale
Mini nun 1 each category
where population >500,000
Major roadway
microscale
—*36,000—
5-15
2-7
or
Major roadway
middle scale
^10,000 20,000 £40,000
>15-50 >15-75 >15-100
2-15
2-15
2-15
High traffic and population density
neiqhborhood scale
510,000
>50
2-15
»,0M
>75
2-15
£40,000
>100
2-15
Source: C.F.R. (1982) 40:§58 App E
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PRELIMINARY DRAFT
TABLE A-Z. TSP NAMS CRITERIA
Approximate Number of Stations Per Area
Population Category
High1
Concentration
Medium2
Low3
High — >500,000
6-8
4-6
0-2
Medium — 100-500,000
4-6
2-4
0-2
Low -- 50-100,000
2-4
1-2
0
lWhen TSP Concentration exceeds by 20% Primary Ambient Air Standard of 75 pg/m3 annual
geometric mean.
2TSP Concentration > Secondary Ambient Air Standard of 60 pg/in3 annual geometric mean.
3TSP Concentration < Secondary Ambient Air Standard.
Source: C.F.R. (1982) 40:§58 App D
With respect to the siting of monitors for lead and other criteria pollutants, there are
standards for elevation of the monitors above ground level, setback fro* roadways, and setback
from obstacles. A summary of the specific siting requirements for lead is presented in Table
4-1 and summarized below:
• Samples must be placed between 2 and 15 meters from the ground and greater than 20
meters from trees.
• Spacing of samplers from roads should vary with traffic volume; a range of 5 to
100 meters from the roadway is suggested.
• Distance from samplers to obstacles must be at least twice the height the obstacle
protrudes above the sampler.
• There must be a 270° arc of unrestricted air flow around the monitor to include
the prevailing wind direction that provides the maximum pollutant concentration to
the monitor.
• No furnaces or incineration flues should be in close proximity to the monitor.
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ZONE C (UNACCEPTABLE)
ZONE A {ACCEPTABLE
=ZONE B (NOT RECOMMENDED)
10
20
DISTANCE FROM EDGE OF NEAREST TRAFFIC LANE, meter*
25
30
Figure 4-1. Acceptable zone for siting TSP monitors where the average daily traffic exceeds 3000
vetiiclas/day.
Zona A: Recommended for neighborhood, urban, regional and most middle spatial scales. All NAMS are In tMs zona.
Zona B: If SLAMS are placed in Zona B they have middle scale of representativeness.
Source: 46 FR 44159-44172
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PRELIMINARY DRAFT
To clarify the relationship between monitoring objectives and the actual siting of a mon-
itor, the concept of a spatial scale of representativeness was developed. The spatial scales
are described in terms of the physical dimensions of the air space surrounding the monitor
throughout which pollutant concentrations are fairly similar. Table 4-3 describes the scales
of representativeness while Table 4-4 relates monitoring objectives to the appropriate spatial
scale.
The time scale may also be an important factor. A study by Lynam (1972) illustrates the
effect of setback distance on short-term (15 minute) measurements of lead concentrations
directly downwind from the source. They found sharp reductions in lead concentration with in-
creasing distance from the roadway. A similar study by PEDCo Environmental, Inc. (1981) did
not show the same pronounced reduction when the data were averaged over monthly or quarterly
time periods. The apparent reason for this effect is that windspeed and direction are not
consistent. Therefore, siting criteria must include sampling times sufficiently long to
include average windspeed and direction, or a sufficient number of samples must be collected
over short sampling periods to provide an average value consistent with a 24-hour exposure.
4.2.2 Ambient Sampling for Particulate and Gaseous lead
Airborne lead is primarily inorganic particulate matter but may occur in the form of
organic gases. Devices used for collecting samples of ambient atmospheric lead include the
standard hi-vol and a variety of other collectors employing filters, impactors, impingers, or
scrubbers, either separately or in combination. Some samplers measure total particulate
matter gravimetrically; thus the lead data are usually expressed in Mfl/fl PM or air.
Other samplers do not measure PM gravimetrically; therefore, the lead data can only be
expressed as mq/d3- Some samplers measure lead deposition expressed In pg/cm2. Some instru-
ments separate particles by size. As a general rule, particles smaller than 2.5 m«i are
defined as fine, and those larger than 2.5 pm are defined as coarse.
In a typical sampler, the ambient air is drawn down Into the inlet and deposited on the
collection surface after one or more stages of particle size separation. Inlet effectiveness,
internal wall losses, and retention efficiency of the collection surface may bias the
collected sample by selectively excluding particles of certain sizes.
4.2.2.1 High Volume Sampler (hi-vol). The present SLAMS and NAMS employ the standard hi-vol
sampler (Robson and Foster, 1962; Silverman and Viles, 1948; U.S. Environmental Protection
Agency, 1971) as part of their sampling networks. As a Federal Reference Method Sampler, the
hi-vol operates with a specific flow rate range of 1.13 to 1.70 m3/min, drawing air through a
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TABLE 4-3, DESCRIPTION OF SPATIAL SCALES OF REPRESENTATIVENESS
Kicroscale
Middle Scale
Neighborhood Scale
Urban Scale
Regional Scale
National and Global
Scales
Defines ambient concentrations In air volumes associated
with areas ranging from several to 100 meters In size.
Defines concentrations in areas from 100 to 500 meters
(area up to several city blocks).
Defines concentrations in an extended area of uniform
land use, within a city, from 0.5 to 4.0 kilometers in
size.
Defines citywide concentrations, areas from 4-10
kilometers in size. Usually requires more than one
site.
Defines concentrations in a rural area with homogeneous
geography. Range of tens to hundreds of kilometers.
Defines concentrations characterizing the U.S. and the
globe as a whole.
Source: C.F.R. (1982) 40:§58 App. D
TABLE 4-4. RELATIONSHIP BETWEEN MONITORING OBJECTIVES AND
APPROPRIATE SPATIAL SCALES
Monitoring objective Appropriate spatial scale for siting air monitors
Highest Concentration
Micro, Middle, Neighborhood (sometimes Urban).
Population
Neighborhood, Urban
Source Impact
Micro, Middle, Neighborhood
General (Background)
Neighborhood, Regional
Source: C.F.R. (1982) 40:§58 App. D
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PRELIMINARY DRAFT
200 x 250 mm glass fiber filter. At these flow rates, 1600 to 2600 m3 of air per day are
sampled. Many hi-vol systews are presently equipped with mass flow sensors to control the
total flow rate through the filter.
The present hi-vol approach has been shown, during performance characterization tests, to
have a number of deficiencies. First, wind tunnel testing by Wedding et al. (1977) has shown
that the inlet characteristics of the hi-vol sampler are strongly affected by particle size,
windspeed, and wind direction. However, since most lead particles have been shown to have a
mass median diameter (HMD) in the range of 0.25 to 1.4 pm (Lee and Goranson, 1972), the hi-vol
sampler should present reasonably good estimates of ambient lead concentrations. However, for
particles greater than 5 p®. the hi-vol system is unlikely to collect representative samples
(McFarland and Rodes, 1979; Wedding et al., 1977). In addition, Lee and Wagnan (1966) and
Stevens et al. (1978) have documented that the use of glass fiber filters leads to the folia-
tion of artifactual sulfate. Spicer et al. (1978) suggested a positive artifactual nitrate,
while Stevens et al. (1980) showed both a positive and negative artifact may occur with glass
or quartz filters when using a hi-vol sampler.
4.2.2.2 Dichotomous Sampler. The dichotomous sampler collects two particle size fractions,
typically 0 to 2.5 pm and 2.5 pm to the upper cutoff of the inlet employed (normally 10 pm).
The impetus for the dichotomy of collection, which approximately separates the fine and coarse
particles, was provided by Whitby et al. (1972) to assist in the identification of particle
sources. A 2.5 pm cutpoint for the separator was also recommended by Miller et al. (1979) be-
cause it satisfied the requirements of health researchers interested in respirable particles,
provided adequate separation between two naturally occurring peaks in the size distribution,
and was mechanically practical. Because the fine and coarse fractions collected in most loca-
tions tend to be acidic and basic, respectively, this separation also minimizes potential par-
ticle interaction after collection.
The particle separation principle used by this sampler was described by Hounam and
Sherwood (1965) and Conner (1966). The version now in use by EPA was developed by Loo et al.
(1979). The separation principle involves acceleration of the particles through a nozzle.
Ninety percent of the flowstream is diverted to a small particle collector, while the larger
particles continue by inertia toward the large particle collection surface. The inertlal
virtual impactor design causes- 10 percent of the fine particles to be collected with the
coarse particle fraction. Therefore, the mass of fine and coarse particles must be adjusted
to allow for their cross contamination. This mass correction procedure has been described by
Dzub^y et al. (1982).
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PRELIMINARY DRAFT
g
Teflon membrane filters with pore sizes as large as 2.0 pm can be used in the dichoto-
mous sampler (Dzubay et al, 1982; Stevens et al., 1980) and have been shown to have essen-
tially 100 percent collection efficiency for particles with an aerodynamic diameter as small
as 0.03 pit (Liu et al., 1976; See Section 4.2.5). Because the sampler operates at a flowrate
of 1 m3/hr (167 1/min) and collects sub-milligram quantities of particles, a microbalance with
a 1 pg resolution is recommended for filter weighing (Shaw, 1980). Removal of the fine par-
ticles via this fractionation technique may result in some of the collected coarse particles
falling off the filter if care is not taken during filter handling and shipping. However,
Dzubay and Barbour (1983) have developed a filter coating procedure which eliminates particle
A
loss during transport. A study by Wedding et al. (1980) has shown that the Sierra inlet to
the dichotomous sampler was sensitive to windspeed. The 50 percent cutpoint (D5o) was found
to vary from 10 to 22 pm over the windspeed range of 0 to 15 km/hr.
Automated versions of the sampler allow timely and unattended changes of the sampler
filters. Depending on atmospheric concentrations, short-term samples of as little as 4 hours
can provide diurnal pattern information. The mass collected during such short sample periods,
however, 1s extremely small and highly variable results may be expected.
4.2.2.3 Impactor Samplers. Impactors provide a means of dividing an ambient particle sample
into subfractions of specific particle size for possible use in determining size distribution.
A jet of air is directed toward a collection surface, which is often coated with an adhesive
or grease to reduce particle bounce. Large, high-inertia particles are unable to turn with
the airstream and consequently hit the collection surface. Smaller particles follow the air-
stream and are directed toward the next impactor stage or to the filter. Use of multiple
stages, each with a different particle size cutpoint, provides collection of particles in
several size ranges.
For determining particle mass, removable impaction surfaces may be weighed before and
after exposure. The particles collected may be removed and analyzed for individual elements.
The selection and preparation of these impaction surfaces have significant effects on the
Impactor performance. Improperly coated or overloaded surfaces can cause particle bounce to
lower stages resulting in substantial cutpoint shifts (Dzubay et al., 1976). Additionally,
coatings may cause contamination of the sample. Marple and Willeke (1976) showed the effect
of various impactor substrates on the sharpness of the stage cutpoint. Glass fiber substrates
can also cause particle bounce or particle Interception (Dzubay et al., 1976) and are subject
to the formation of artifacts, due to reactive gases interacting with the glass fiber, similar
to those on hi-vol sampler filters (Stevens et al., 1978).
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Cascade impactors typically have 2 to 10 stages, and flowrates for commercial low-volume
versions range from about 0.01 to 0.10 m3/min. Lee and Goranson (1972) modified a commer-
cially available 0.03 m3/min low-volume impactor and operated it at 0.14 m3/min to obtain
larger mass collections on each stage. Cascade impactors have also been designed to mount on
a hi-vol sampler and operate at flowrates as high as 0.6 to 1.1 m3/min.
Particle size cutpoints for each stage depend primarily on sampler geometry and flowrate.
The smallest particle size cutpoint routinely used is approximately 0.3 jjm, although special
low-pressure impactors such as that described by Bering et al. (1978) are available with cut-
points as small as 0.05 ym. However, due to the low pressure, volatile organics and nitrates
are lost during sampling. A membrane filter is typically used after the last stage to collect
the remaining small particles.
4.2.2.4 Dry Deposition Sampling. Dry deposition may be measured directly with surrogate or
natural surfaces, or indirectly using micrometeorological techniques. The earliest surrogate
surfaces were dustfall buckets placed upright and exposed for several days. The HASL wet-dry
collector is a modification which permits one of a pair of buckets to remain covered except
during rainfall. These buckets do not collect a representative sample of particles in the
small size range where lead is found because the rim perturbs the natural turbulent flow of
the main airstream (Hicks et al., 1980). They are widely used for other pollutants, espe-
cially large particles, in the National Atmospheric Deposition Program.
Other surrogate surface devices with smaller rims or no rims have been developed recently
(Elias et al., 1976; Lindberg et al., 1979; Peirson et al., 1973). Peirson et al. (1973)
used horizontal sheets of filter paper exposed for several days with protection from rainfall.
Elias et al. (1976) used Teflon® disks held rigid with a 1 cm Teflon® ring. Lindberg et al,
(1979) used petri dishes suspended in a forest canopy. In all of these studies, the calcu-
lated deposition velocity (see Section 6.3.1) was within the range expected for small aerosol
particles.
A few studies have measured direct deposition on vegetation surfaces using chemical wash-
ing techniques to remove surface particles. These determinations are generally 4 to 10 times
lower than comparable surrogate surface measurements (Elias et al., 1976; Lindberg et al.,
1979), but the reason for this difference could be that natural surfaces represent net accumu-
lation rather than total deposition. Lead removed by rain or other processes would show an
apparently lower deposition rate.
There are several micrometeorological techniques that have been used to measure particle
deposition. They overcome the major deficiency of surrogate surfaces, the lack of correlation
between the natural and artificial surfaces, but micrometeorological techniques require expen-
sive equipment and skilled operators. They measure instantaneous or short-term deposition
023PB4/A
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preliminary Draft
only, and this deposition is inferred to be to a plane projected surface area only, not neces-
sarily to vegetation surfaces.
Of the five mi crometeorological techniques commonly used to measure particle deposition,
only two have been used to measure lead particle deposition. Everett et al. (1979) used the
profile gradient technique by which lead concentrations are measured at two or more levels
within 10 m above the surface, Parallel meteorological data are used to calculate the net
flux downward. Droppo (1980) used eddy correlation, which measures fluctuations in the ver-
tical wind component with adjacent measurements of lead concentrations. The calculated dif-
ferences of each can be used to determine the turbulent flux. These two micrometeorological
techniques and the three not yet used for lead, modified Bowen. variance, and eddy accumula-
tion. are described in detail in Hicks et al. (1980).
4.2.2.5 Gas Collection. When sampling ambient lead with systems employing filters, it is
likely that vapor-phase organolead compounds will pass through the filter media. The use of
bubblers downstream of the filter containing a suitable reagent'or absorber for collection of
these compounds has been shown to be effective (Purdue et al., 1973). Organolead may be col-
lected on iodine crystals, adsorbed on activated charcoal, or absorbed in an iodine mono-
chloride solution (Skogerboe et al., 1977b).
In one experiment, Purdue et al. (1973) operated two buhblers in series containing iodine
monochloride solution. One hundred percent of the lead was recovered in the first bubbler.
It should be noted, however, that the analytical detection sensitivity was poor. In general,
use of bubblers limits the sample volume due to losses by evaporation and/or bubble carryover.
4.2.3 Source Sampling
Sources of lead include automobiles, smelters, coal-burning facilities, waste oil combus-
tion, battery manufacturing plants, chemical processing plants, facilities for scrap proces-
sing, and welding and soldering operations (see Section 5.3.3). A potentially important
secondary source is fugitive dust from mining operations and from soils contaminated with
automotive emissions (Olson and Skogerboe, 1975). Chapter 5 contains a complete discussion of
sources of lead emissions. The following sections discuss the sampling of stationary and
mobile sources.
4.2.3.1 Stationary Sources. Sampling of stationary sources for lead requires the use of a
sequence of samplers at the source of the effluent stream. Since lead in stack emissions nay
be present in a variety of physical and chemical forms, source sampling trains must be de-
signed to trap and retain both gaseous and particulate lead. A sampling probe is inserted
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PRELIMINARY DRAFT
directly in the stack or exhaust streaii. In the tentative ASTM method for sampling for atmos-
pheric lead, air is pulled through a 0.45 pm membrane filter and an activated carbon adsorp-
tion tube (American Society for Testing and Materials, 1975a). In a study of manual methods
for measuring emission concentrations of lead and other toxic materials, Coulson et al.
(1973), recommended use of a filter, a system of impingers, a metering system, and a pump.
4.2.3.2 Mobile Sources. Three principal procedures have been used to obtain samples of auto
exhaust aerosols for subsequent analysis for lead compounds: a horizontal dilution tunnel,
plastic sample collection bags and a low residence tine proportional sampler. In each proce-
dure, samples are air diluted to simulate roadside exposure conditions. In the most commonly
used procedure, a large horizontal air dilution tube segregates fine combustion-derived parti-
cles from larger lead particles ablated from combustion chamber and exhaust deposits. In this
procedure, hot exhaust is ducted into a 56-cm diameter, 12-m long, air dilution tunnel and
mixed with filtered ambient air in a 10-cm diameter mixing baffle in a concurrent flow
arrangement. Total exhaust and dilution airflow rate is 28 to 36 mVmin, which produces a
residence time of approximately 5 sec in the tunnel. At the downstream end of the tunnel,
samples of the aerosol are obtained by means of isokinetic probes using filters or cascade
impactors (Habibi, 1970).
In recent years, various configurations of the horizontal air dilution tunnel have been
developed. Several dilution tunnels have been made of polyvinyl chloride with a diameter of
46 cm, but these are subject to wall losses due to charge effects (Gentel et al., 1973; Moran
et al., 1972; Trayser et al., 1975). Such tunnels of varying lengths have been limited by
exhaust temperatures to total flows above approximately 11 m3/min. Similar tunnels have a
centrifugal fan located upstream, rather than a positive displacement pump located downstream
(Trayser et al., 1975). This geometry produces a slight positive pressure in the tunnel and
expedites transfer of the aerosol to holding chambers for studies of aerosol growth. However,
turbulence from the fan may affect the sampling efficiency. Since the total exhaust plus
dilution airflow is not held constant in this system, potential errors can be reduced by main-
taining a very high dilution air/exhaust flow ratio (Trayser et al., 1975).
There have also been a number of studies using total filtration of the exhaust stream to
arrive at material balances for lead with rather low back-pressure metal filters in an air
distribution tunnel (Habibi, 1973; Hirschler et al., 1957; Hirschler and Gilbert, 1964;
Sampson and Springer, 1973). The cylindrical filtration unit used in these studies is better
than 99 percent efficient in retaining lead particles (Habibi, 1973). Supporting data for
lead balances generally confirm this conclusion (Kunz et al., 1975).
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In the bag technique, auto emissions produced during simulated driving cycles are air-
diluted and collected 1n a large plastic bag. The aerosol sample 1s passed through a filtra-
tion or Impaction sampler prior to lead analysis (Ter Haar et al., 1972). This technique may
result in errors of aerosol size analysis because of condensation of low vapor pressure
organic substances onto the lead particles.
To minimize condensation problems, a third technique, a low residence time proportional
sampling system, has been used. It is based on proportional sampling of raw exhaust, again
diluted with ambient air followed by filtration or impaction (Ganley and Springer, 1974;
Sampson and Springer, 1973). Since the sample flow must be a constant proportion of the total
exhaust flow, this technique may be limited by the response time of the equipment to operating
cycle phases that cause relatively small transients in the exhaust flow rate.
4.2.4 Sampling for Lead 1n Other Media
Other primary environmental media that may be affected by airborne lead include precipi-
tation, surface water, soil, vegetation, and foodstuffs. The sampling plans and the sampling
methodologies used in dealing with these media depend on the purpose of the experiments, the
types of measurements to be carried out, and the analytical technique to be used. General
approaches are given below in lieu of specific procedures associated with the numerous possi-
ble special situations.
4.2.4.1 Precipitation. The investigator should be aware that dry deposition occurs continu-
ously, that lead at the start of a rain event is higher in concentration than at the end, and
that rain striking the canopy of a forest may rinse dry deposition particles from the leaf
surfaces. Rain collection systems should be designed to collect precipitation on an event
basis and to collect sequential samples during the event. They should be tightly sealed from
the atmosphere before and after sampling to prevent contamination from dry deposition, falling
leaves, and flying Insects. Samples should be acidified to pH 1 with nitric acid and refrig-
erated immediately after sampling. All collection and storage surfaces should be thoroughly
cleaned and free of contamination.
Two automated systems have been in use for some time. The Sangamo Precipitation
Collector, Type A, collects rain in a single bucket exposed at the beginning of the rain event
(Samant and Vaidya, 1982). These authors reported no leaching of lead from the bucket into a
solution of 0.3N HN03. A second sampler, described by Coscio et al. (1982), also remains
covered between rain events; it can collect a sequence of eight samples during the period of
rain and may be fitted with a refrigeration unit for sample cooling. No reports of lead
analyses were given. Because neither system 1s widely used, their monitoring effectiveness
has not been thoroughly evaluated.
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4.2.4.2 Surface Water. Atmospheric lead may be dissolved in water as hydrated ions, chemical
complexes, and soluble compounds, or it may be associated with suspended matter. Because the
physicochemical form often influences environmental effects, there is a need to differentiate
among the various chemical forms of lead. Complete differentiation among all such forms is a
complex task that has not yet been fully accomplished. The most commonly used approach is to
distinguish between dissolved and suspended forms of lead. All lead passing through a 0.45 pi
membrane filter is operationally defined as dissolved, while that retained on the filter is
defined as suspended (Kopp and HcKee, 1979).
When sampling water bodies, flow dynamics should be considered in the context of the pur-
pose for which the sample is collected. Water at the convergence point of two flowing
streams, for example, may not be well mixed for several hundred meters. Similarly, the heavy
metal concentrations above and below the thermocline of a lake may be very different. Thus,
several samples should be selected in order to define the degree of horizontal or vertical
variation. The final sampling plan should be based on the results of pilot studies. In cases
where the average concentration is of primary concern, samples can be collected at several
points and then mixed to obtain a composite.
Containers used for sample collection and storage should be fabricated from essentially
lead-free plastic or glass, e.g., conventional polyethylene, Teflon®, or quartz. These con-
tainers must be leached with hot acid for several days to ensure minimum lead contamination
(Patterson and Settle, 1976). If only the total lead is to be determined, the sample may be
collected without filtration in the field. Nitric acid should be added immediately to reduce
the pH to less than 2 (U.S. Environmental Protection Agency, 1978). The acid will normally
dissolve the suspended lead. Otherwise, it is recommended that the sample be filtered upon
collection to separate the suspended and dissolved lead and the latter preserved by acid addi-
tion as above. It is also recommended that water samples be stored at 4°C until analysis to
avoid further leaching from the container wall (Fishman and Erdmann, 1973; Kopp and Kroner,
1967; Lovering, 1976; National Academy of Sciences, 1972; U.S. Environmental Protection
Agency, 1978).
4.2.4.3 Soils. The distance and depth gradients associated with lead in soil from emission
sources must be considered in designing the sampling plan. Beyond that, actual sampling is
not particularly complex (Skogerboe et al., 1977b). Vegetation, litter, and large objects
such as stones should not be included in the sample. Depth samples should be collected at 2
on intervals to preserve vertical integrity. The samples should be air dried and stored in
sealed containers until analyzed.
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4.2.4.4 Vegetation. Because most soil lead is in forms unavailable to plants, and because
lead is not easily transported by plants, roots typically contain very little lead and shoots
even less (Zimdahl, 1976; Zimdahl and Koeppe, 1977). Before analysis, a decision oust be made
as to whether or not the plant material should be washed to remove surface contamination front
dry deposition and soil particles. If the plants are sampled for total lead content (e.g., if
they serve as animal food sources), they cannot be washed. If the effect of lead on internal
plant processes is being studied, the plant samples should be washed. In either case, the
decision must be made at the time of sampling, as washing cannot be effective after the plant
materials have dried. Fresh plant samples cannot be stored for any length of time in a
tightly closed container before washing because molds and enzymatic action may affect the dis-
tribution of lead on and in the plant tissues. Freshly picked leaves stored in sealed poly-
ethylene bags at room temperature generally begin to decompose in a few days. Storage time
may be increased to approximately 2 weeks by refrigeration.
After collection, plant samples should be dried as rapidly as possible to minimize chem-
ical and biological changes. Samples that are to be stored for extended periods of time
should be oven dried to arrest enzymatic reactions and render the plant tissue amenable to
grinding. Storage in sealed containers is required after grinding. For analysis of surface
lead, fresh, intact plant parts are agitated in dilute nitric acid or EOTA solutions for a few
seconds.
4.2.4.5 Foodstuffs. From 1972 to 1978, lead analysis was included in the Food and Drug
Administration Market Basket Survey, which involves nationwide sampling of foods representing
the average diet of an 18-year-old male, i.e., the individual who on a statistical basis eats
the greatest quantity of food (Kolbye et al., 1974). Various food items from the several food
classes are purchased in local markets and made up into meal composites in the proportion that
each food item is ingested; they are then cooked or otherwise prepared as they would be con-
sumed. Foods are grouped into 12 food classes, then composited and analyzed chemically.
Other sampling programs may be required for different investigative purposes. For those foods
where lead may be deposited on the edible portion, the question of whether or not to use
typical kitchen washing procedures before analysis should be considered in the context of the
experimental purpose.
4.2.5 Filter Selection and Sample Preparation
In sampling for airborne lead, air is drawn through filter materials such as glass fiber,
cellulose acetate, or porous plastic (Skogerboe et al., 1977b, Stern, 1968). These materials
often include contaminant lead that can interfere with the subsequent analysis (Gandrud and
Lazrus, 1972; Kometani et al. 1972; Luke et al., 1972; Seeley and Skogerboe, 1974). If the
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saaple collected is large, then the effects of these trace contaminants may be negligible
(Witz and MacPhee, 1976). Procedures for cleaning filters to reduce the lead blank rely on
washing with acids or conplexing agents (Gandrud and Lazrus, 1972). The type of filter and
the analytical method to be used often determines the ashing technique. In some methods,
e.g., X-ray fluorescence, analysis can be performed directly on the filter if the filter
material is suitable (Dzubay and Stevens, 1975). Skogerboe (1974) provided a general review
of filter materials.
The main advantages of glass fiber filters are low pressure drop and high particle col-
lection efficiency at high flow rates. The main disadvantage is variable lead blank, which
makes their use inadvisable in many cases (Kometani et al., 1972; Luke at al., 1972). This
has placed a high priority on the standardization of a suitable filter for hi-vol samples
(Witz and MacPhee, 1976). Other investigations have indicated, however, that glass fiber
filters are now available that do not present a lead interference problem (Scott et al.,
1976b). Teflon® filters have been used since 1975 by Dzubay et al. (1982) and Stevens et al.
(1978), who have shown these filters to have very low lead blanks (<2 ng/cm2). The collection
efficiencies of filters, and also of Impactors, have been shown to be dominant factors in the
quality of the derived data (Skogerboe et al., 1977a).
Sample preparation usually involves conversion to a solution through wet ashing of solids
with acids or through dry ashing in a furnace followed by acid treatment. Either approach
works effectively if used properly (Kometani et al., 1972; Skogerboe et al., 1977b). In one
investigation of porous plastic Nuclepore8 filters, some lead blanks were too high to allow
measurements of ambient air lead concentrations (Skogerboe et al., 1977b).
4.3 ANALYSIS
The choice of analytical method depends on the nature of the data required, the type of
sample being analyzed, the skill of the analyst, and the equipment available. For general
determination of elemental lead, atomic absorption spectroscopy is widely used and recommended
[40 C.F.R. (1982) 40:§50]. Optical emission spectrometry (Scott et al., 1976b) and X-ray
fluorescence (Stevens et al., 1978) are rapid and inexpensive methods for multielemental
analyses. X-ray fluorescence can measure lead concentrations reliably to 1 ng/ms using sam-
ples collected with commercial dichotomous samplers. Other analytical methods have specific
advantages appropriate for special studies. Only those analytical techniques receiving wide-
spread current use in lead analysis are described below. More complete reviews are available
in the literature (American Public Health Association, 1971; Lovering, 1976; Skogerboe et al.,
1977b; National Academy of Sciences, 1980).
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With respect to measuring lead without sampling or laboratory contamination, several in-
vestigators have shown that the magnitude of the problem is quite large (Patterson and Settle,
1976; Patterson et al., 1976; Pierce et ah, 1976; Patterson, 1982; Skogerboe, 1982). It
appears that the problem may be caused by failure to control the blank or by failure to stan-
dardize instrument operation (Patterson, 1982; Skogerboe, 1982). The laboratory atmosphere,
collecting containers, and the labware used may be primary contributors to the lead blank pro-
blem (Murphy, 1976; Patterson, 1982; Skogerboe, 1982). Failure to recognize these and other
sources such as reagents and hand contact is very likely to result in the generation of arti-
ficially high analytical results. Samples with less than 100 pg Pb should be analyzed in a
clean laboratory especially designed for the elimination of lead contamination. Moody (1982)
has described the construction and application of such a laboratory at the National Bureau of
Standards.
For many analytical techniques, a preconcentration step is recommended. Leyden and
Wegschelder (1981) have described several procedures and the associated problems with control-
ling the analytical blank. There are two steps to preconcentration. The first is the removal
of organic matter by dry ashing or wet digestion. The second is the separation of lead from
interfering metallic elements by copredpitation or passing through a resin column. New sepa-
ration techniques are continuously being evaluated, many of which have application to specific
analytical problems. Yang and Yeh (1982) have described a polyacrylamide-hydrous-zirconia
(PHZ) composite ion exchanger suitable for high phosphate solutions. Corsini, et al. (1982)
evaluated a macroreticular acrylic ester resin capable of removing free and inorganically
bound metal ions directly from aqueous solution without prior chelation.
4.3.1 Atomic Absorption Spectroscopy (AAS)
Atomic absorption spectroscopy (AAS) is a widely accepted method for the measurement of
lead in environmental sampling (Skogerboe et al., 1977b). A variety of lead studies using AAS
have been reported (Kometani et al., 1972; Zoller et al., 1974; Huntzicker et al., 1975; Scott
et al., 1976b; Lester et al., 1977; Hirao et al., 1979; Compton and Thomas, 1980; Bertenshaw
and Gelsthorpe, 1981).
The lead atoms in the sample must be vaporized either in a precisely controlled flame or
in a furnace. Furnace systems in AAS offer high sensitivity as well as the ability to analyze
small samples (Lester et al., 1977; Rouseff and Ting, 1980; Stein et al., 1980; Bertenshaw et
al., 1981). These enhanced capabilities are offset In part by greater difficulty in analyti-
cal calibration and by loss of analytical precision.
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Pachuta and Love (1980) collected particles on cellulose acetate filters. Disks (0.5
on2) were punched from these filters and analyzed by insertion of the nichrome cups containing
the disks into a flame. Another application involves the use of graphite cups as particle
filters with the subsequent analysis of the cups directly in the furnace system (Seeley and
Skogerboe, 1974; Torsi et al., 1981). These two procedures offer the ability to determine
particulate lead directly with minimal sample handling.
In an analysis using AAS and hi-vol samplers, atmospheric concentrations of lead were
3
found to be 0.076 ng/m at the South Pole (Maenhaut et al., 1979). Lead analyses of 995 par-
ticulate samples from the NASN were accomplished by AAS with an indicated precision of 11
percent (Scott et al., 1976a, see also Section 7.2.1.1). More specialized AAS methods for the
determination of tetraalkyl lead compounds in water and fish tissue have been described by
Chau et al. (1979) and in air by Birnie and Noden (1980) as well as Rohbock et al. (1980).
Atomic absorption requires as much care as other techniques to obtain highly precise
data. Background absorption, chemical interference, background light loss, and other factors
can cause errors. A major problem with AAS is that untrained operators use it in many labor-
atories without adequate quality control.
Techniques for AAS are still evolving. An alternative to the graphite furnace, evaluated
by Jin and Taga (1982), uses a heated quartz tube through which the metal ion in gaseous
hydride form flows continuously. Sensitivities were 1 to 3 ng/g for lead. The technique is
similar to the hydride generators used for mercury, arsenic, and selenium. Other nonflame
atomization systems, electrodeless discharge lamps, and other equipment refinements and tech-
nique developments have been reported (Horlick, 1982).
4.3.2 Emission Spectroscopy
Optical emission spectroscopy 1s based on the measurement of the light emitted by
elements when they are excited in an appropriate energy medium. The technique has been used
to determine the lead content of soils, rocks, and minerals at the 5 to 10 Mfl/g level with a
relative standard deviation of 5 to 10 percent (Anonymous, 1963); this method has also been
applied to the analysis of a large number of air samples (Scott et al., 1976b; Suglmae and
Skogerboe, 1978). The primary advantage of this method is that it allows simultaneous meas-
urement of a large number of elements in a small sample (Ward and Fishman, 1976).
In a study of environmental contamination by automotive lead, sampling times were short-
ened by using a sampling technique in which lead-free porous graphite was used both as the
filter medium and as the electrode in the spectrometer (Copeland et al., 1973; Seeley and
Skogerboe, 1974). Lead concentrations of 1 to 10 were detected after a half-hour flow
at 800 to 1200 ml/min through the filter.
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Scott et al. (1976a) analyzed composited particulate samples obtained with hi-vols for
about 24 elements, including lead, using a direct reading emission spectrometer. Over 1000
samples collected by the NASN In 1970 were analyzed. Careful consideration of accuracy and
precision led to the conclusion that optical emission spectroscopy is a rapid and practical
technique for particle analysis.
More recent activities have focused attention on the inductively coupled plasma (ICP)
system as a valuable means of excitation and analysis (Garbarino and Taylor, 1979; Winge et
al., 1977). The ICP system offers a higher degree of sensitivity with less analytical inter-
ference than is typical of many of the other emission spectroscopic systems. Optical emission
methods are inefficient when used for analysis of a single element, since the equipment is
expensive and a high level of operator training is required. This problem is largely offset
when analysis for several elements is required as is often the case for atmospheric aerosols.
4.3.3 X-Ray Fluorescence (XRF)
X-ray emissions that characterize the elemental content of a sample also occur when atoms
are irradiated at sufficient energy to excite an inner-shell electron (Hammerle and Pierson,
1975; Jaklevic et al., 1973; Skogerboe et al., 1977b; Stevens et al., 1978). This fluores-
cence allows simultaneous identification of a range of elements including lead.
X-ray fluorescence may require a high-energy irradiation source. But with the X-ray
tubes coupled with fluorescers (Jaklevic et al., 1973; Dzubay and Stevens, 1975; Paciga and
Jervis, 1976) very little energy is transmitted to the sample, thus sample degradation is kept
to a minimum (Shaw et al., 1980). Electron beams (McKinley et al., 1966), and radioactive
isotope sources (Kneip and Laurer 1972) have been used extensively (Birks et al., 1971; Birks,
1972) as energy sources for XRF analysis. To reduce background interference, secondary fluor-
escers have been employed (Birks et al., 1971; Dzubay and Stevens, 1975). The fluorescent
X-ray emission from the sample may be analyzed with a crystal monochromator and detected with
scintillation or proportional counters (Skogerboe et al., 1977b) or with low-temperature semi-
conductor detectors that discriminate the energy of the fluorescence. The latter technique
requires a very low level of excitation (Dzubay and Stevens, 1975; Toussaint and Boniforti,
1979).
X-ray emission induced by charged-particle excitation (proton-induced X-ray emission or
PIXE) offers an attractive alterative to the more common techniques (Barfoot et al., 1979;
Hardy et al., 1976; Johansson et al., 1970). Recognition of the potential of heavy-particle
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bombardment for excitation was demonstrated by Johansson et al. (1970), who reported an inter-
ference-free signal in the picogram (10 12 g) range. The excellent capability of accelerator
beams for X-ray emission analysis is partially due to the relatively low background radiation
associated with the excitation. The high particle fluxes obtainable from accelerators also
contribute to the sensitivity of the PIXE method. Literature reviews (Folkmann et al., 1974;
Gi If rich et al., 1973; Herman et al., 1973; Walter et al., 1974) on approaches to X-ray
elemental analysis agree that protons of a few MeV energy provide a preferred combination for
high sensitivity analysis under conditions less subject to matrix interference effects. As a
result of this premise, a system designed for routine analysis has been described (Johansson
et al., 1975) and papers involving the use of PIXE for aerosol analysis have appeared (Hardy
et al., 1976; Johansson et al., 1975). The use of radionuclides to excite X-ray fluorescence
and to determine lead in airborne particles has also been described (Havranek and Bumbalova,
1981; Havranek et al., 1980).
X-radiation is the basis of the electron microprobe method of analysis. When an intense
electron beam is incident on a sample, it produces several forms of radiation, including
X-rays, whose wavelengths depend on the elements present in the material and whose intensities
depend on the relative quantities of these elements. An electron beam that gives a spot size
as small as 0.2 m® is possible. The microprobe is often incorporated in a scanning electron
microscope that allows precise location of the beam and comparison of the sample morphology
with its elemental composition. Under ideal conditions, the analysis is quantitative, with an
accuracy of a few percent. The mass of the analyzed element may range from 10 14 to 10 16 g
(McKinley et al., 1966).
Electron microprobe analysis is not a widely applicable monitoring method. It requires
expensive equipment, complex sample preparation procedures, and a highly trained operator.
The method is unique, however, in providing compositional information on Individual lead par-
ticles, thus permitting the study of dynamic chemical changes and perhaps allowing improved
source identification.
Advantages of X-ray fluorescence methods include the ability to detect a variety of
elements, the ability to analyze with little or no sample preparation, low detection limits (2
ng Pb/m3) and the availability of automated analytical equipment. Disadvantages are that the
X-ray analysis requires liquid nitrogen (e.g., for energy-dispersive models) and highly
trained analysts. The detection limit for lead is approximately 9 ng/cm2 of filter area
(Jaklevic and Walter, 1977), which is well below the quantity obtained in normal sampling
periods with the dichotomous sampler (Dzubay and Stevens, 1975).
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4.3.4 Mass Spectrometry
Isotope dilution mass spectrometry (IDMS) is an absolute measurement technique. It
serves as the standard to which other analytical techniques are compared. No other techniques
serve more reliably as a comparative reference. Its use for analyses at subnanogram concen-
trations of lead and in a variety of sample types has been reported (Chow et al., 1969, 1974;
Facchetti and Geiss, 1982; Hirao and Patterson, 1974; Murozumi et al., 1969; Patterson et al.,
1976; Rabinowitz et al., 1973).
The isotopic composition of lead peculiar to various ore bodies and crustal sources may
also be used as a means of tracing the origin of anthropogenic lead. Other examples of IDMS
application are found in several reports cited above, and in Rabinowitz and Wetherill (1972),
Stacey and Kramers (1975), and Machlan et al. (1976).
4.3.5 Colorimetric Analysis
Colorimetrlc or spectrophotometry analysis for lead using dithizone (diphenylthiocarba-
zone) as the reagent has been used for many years (Anonymous, 1963; Horowitz et al., 1970;
Sandell, 1944). It was the primary method recommended by a National Academy of Sciences
(1972) report on lead, and the basts for the tentative method of testing for lead in the
atmosphere by the American Society for Testing and Materials (1975b). Prior to the
development of the IDMS method, colorimetric analysis served as the reference by which other
methods were tested.
The procedures for the colorimetric analysis require a skilled analyst if reliable
results are to be obtained. The ASTM conducted a collaborative test of the method (Foster et
al., 1975) and concluded that the procedure gave satisfactory precision in the determination
of particulate lead In the atmosphere. In addition, the required apparatus is simple and
relatively inexpensive, the absorption is linearly related to the lead concentration, large
samples can be used, and interferences can be removed (Skogerboe et al., 1977b). Realization
of these advantages depends on meticulous attention to the procedures and reagents.
4.3.6 Electrochemical Methods: Anodic Stripping Voltammetrv (ASV), Differential Pulse
Polarography (DPP)
BMW—
Analytical methods based on electrochemical phenomena are found in a variety of forms
(Sawyer and Roberts, 1974; Willard et al., 1974). They are characterized by a high degree of
sensitivity, selectivity, and accuracy derived from the relationship between current, charge,
potential, and time for electrolytic reactions in solutions. The electrochemistry of lead is
based primarily on Pb(II), which behaves reversibly in Ionic solutions having a reduction po-
tential near -0.4 volt versus the standard calomel electrode (Skogerboe et al., 1977b). Two
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• ' \ .
electrochemical methods generally offer sufficient analytical sensitivity for most lead mea-
surement problems. Differential pulse polarography (DPP) relies on the measurement of the
faradaic current for lead as the voltage is scanWd"While compensating for the nonfaradaic
(background) current produced (McDonnell, 1981). Anodic stripping voltamnetry (ASV) is a two
step process in which the lead is preconcentrated onto a mercury electrode by an extended but
selected period of reduction. After the reduction step, the potential is scanned either
linearly or by differential pulse to oxidize the lead and allow measurement of the oxidation
(stripping) current. The preconcentration step allows development of enhanced analytical
signals; when used in combination with the differential pulse method lead concentrations at
the subnanogram level can be measured (Florence, 1980).
The ASV method has been widely applied to the analysis of atmospheric lead (Harrison et
al., 1971; Khandekar et al., 1981; MacLeod and Lee, 1973). Landy (1980) has shown the applic-
ability to the determination of Cd, Cu, Pb, and Zn in Antarctic snow while Nguyen et al.
(1979) have analyzed rain water and snow samples. Green et al. (1981) have used the method to
determine Cd, Cu, and Pb in sea water. The ASV determination of Cd, Cu, Pb, and Zn in foods
has been described by Jones et al., 1977; Mannino, 1982; and Satzger et al., 1982, and the
general accuracy of the method summarized by Holak (1980). Current practice with commercially
available equipment allows lead analysis at subnanogram concentrations with precision at the 5
to 10 percent on a routine basis (Skogerboe et al., 1977b). New developments center around
the use of microcomputers in controlling the stripping voltage (Kryger, 1981) and conforma-
tional modifications of the electrode (Brihaye and Duyckaerts, 1982).
4.3.7 Methods for Compound Analysis
The majority of analytical methods are restricted to measurement of total lead and cannot
directly identify the various compounds of lead. The electron microprobe and other X-ray
fluorescence methods provide approximate data on compounds on the basis of the ratios of
elements present (Ter Haar and Bayard, 1971). Gas chromatography (GC) using the electron cap-
ture detector has been demonstrated to be useful for organolead compounds (Shapiro and Frey,
1968). The use of atomic absorption as the GC detector for organolead compounds has been
described by DeJonghe et al. (1981), while a plasma emission detector has been used by Estes
et al. (1981). In addition, Messman and Rains (1981) have used liquid chromatography with an
atomic absorption detector to measure organolead compounds. Mass spectrometry may also be
used with gas chromatography (Mykytiuk et al., 1980).
Powder X-ray diffraction techniques have been applied to the identification of lead com-
pounds in soils by Olson and Skogerboe (1975) and by Linton et al. (1980). X-ray diffraction
techniques were used (Harrison and Perry, 1977; Foster and Lott, 1980; Jacklevic et al., 1981)
to identify lead compounds collected on air filters.
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4.4 CONCLUSIONS
To monitor lead particles in air, collection with the hi-vol and dichotomous samplers and
analysis by atomic absorption spectrometry and X-ray fluorescence methods have emerged as the
most widely used methods. Sampling with the hi-vol has inherent biases in sampling large par-
ticles and does not provide for fractionation of the particles according to size, nor does it
allow determination of the gaseous (organic) concentrations. Sampling with a dichotoaous
sampler provides size information but does not allow for gaseous lead measurements. The size
distribution of lead aerosol particles is important in considering inhalable particulate
matter. To determine gaseous lead, it is necessary to back up the filter with chemical
scrubbers such as a crystalline iodine trap.
X-ray fluorescence and optical emission spectroscopy are applicable to multi-element
analysis. Other analytical techniques find application for specific purposes. The paucity of
data on the types of lead compounds at sub nanogram levels in the ambient air is currently
being addressed through development of improved XRF analyzer procedures.
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4.5 REFERENCES
\
American Public Health Association. (1971) Standard methods for the examination of water and
wastewater; 13th Ed. New York, NY: American Public Health Association.
American Society for Testing and Materials. (1975a) Standard method for collection and analy-
sis of dustfall (settleable particulates); D 1739-70. Annu. Book ASTM Stand. 1975:
517-521.
American Society for Testing and Materials. (1975b) Tentative method of test for lead in the
atmosphere by colorlmetric dithizone procedure; D 3112-72T. Annu. Book ASTM Stand. 1975:
633-641.
Anonymous. (1963) Official standardized and recommended methods of analysis. Cambridge, MA:
W. Heffer and Sons, Ltd.
Barfoot, K. M.; Mitchell, I. V.; Eschbach, H. L.; Mason, P. I.; Gil boy, W. B. (1979) The anal-
ysis of air particulate deposits using 2 MeV protons. J. Radioanal. Chen. 53: 255-271.
Bertenshaw, M. P,; Gelsthorpe, D. (1981) Determination of lead in drinking water by atomic-
absorption spectrophotometry with electrothermal atomisation. Analyst (London) 106:
23-31.
Birks, L. S. (1972) X-ray absorption and emission. Anal. Chem. 44: 557R-562R.
Birks, L. S,; Gilfrich, J. V.; Nagel, D. J. (1971) Large-scale monitoring of automobile
exhaust particulates: methods and costs. Washington, DC: Naval Research Laboratory; NRL
memorandum report 2350. Available from: NTIS, Springfield, VA; AD 738801.
Birnie, S. E.; Noden, F. G. (1980) Determination of tetramethyl- and tetraethyllead vapours in
air following collection on a glass-fibre-iodised carbon filter disc. Analyst (London)
105: 110-118.
Brihaye, C.; Duyckaerts, G. (1982) Determination of traces of metals by anodic stripping volt-
amnetry at a rotating glassy carbon ring-disc electrode. Part I: Method and instrumenta-
tion with evaluation of some parameters. Anal. Chin. Acta 143: 111-120.
C.F.R. (1982) 40:§50; National primary and secondary ambient air quality standards.
C.F.R. (1982) 40:§58; Ambient air quality surveillance.
Chau, Y. K.; Wong, P. T. S.; Bengert, G. A.; Kramar, 0. (1979) Determination of tetraalkyl
lead compounds in water, sediment, and fish samples. Anal. Chem. 51: 186-188.
Chow, T. J.; Earl, J. L.; Bennet, C. F. (1969) Lead aerosols in marine atmosphere. Environ.
Sci. Technol. 3: 737-742.
Chow, T. J.; Patterson, C. C.; Settle, D. (1974) Occurrence of lead in tuna [Letter]. Nature
(London) 251: 159-161.
Compton, R. 0.; Thomas, L. A, (1980) Analysis of air samples for lead and manganese. Tex.
J. Sci. 32: 351-355.
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Conner, W. D. C1966) An inertial-type particle separator for collecting large samples. J. Air
Pollut. Control Assoc. 16: 35-38.
Copeland, T. R.; Christie, J, H.; Skogerboe, R. K.; Osteryoung, R. A. (1973) Effect of
supporting electrolyte concentration in pulsed stripping voltammetry at the thin film
mercury electrode. Anal. Chen. 45: 995-996.
Corsinl, A.; Chiang, S.; Difruscia, R. (1982) Direct preconcentration of trace elements in
aqueous solutions on macroreticular acrylic ester resin. [Letter] Anal. Chen. 54:
1433-1435.
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PRELIMINARY DRAFT
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B04REF/A
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PRELIMINARY DRAFT
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B04REF/A
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PRELIMINARY DRAFT
5. SOURCES AND EMISSIONS
5.1 HISTORICAL PERSPECTIVE
The history of global lead emissions has been assembled from chronological records of
deposition in polar snow strata, marine and freshwater sediments, and the annual rings of
trees. These records are important for two reasons. They aid in establishing natural
background levels of lead in air, soils, plants, animals, and humans. They also place current
trends in atmospheric lead concentrations in the perspective of historical changes. Most
chronological records document the sudden increase in atmospheric lead at the time of the
Industrial revolution, and a later burst during the 1920's when lead-alkyls were first added
to gasoline.
Tree ring analyses are not likely to show the detailed year-by-year chronological record
of atmospheric lead Increases. In situations where ring porous tree species that retain the
nutrient solution only 1n the most recent annual rings are growing in heavily polluted areas
where soil lead has increased 100-fold, significant increases in the lead content of tree
rings over the last several decades have been documented. Rolfe (1974) found 4-fold increases
in both rural and urban tree rings using pooled samples from the period of 1910-20 compared to
samples from the period from 1963-73. Symeonides (1979) found a 2-fold increase during a
comparable interval at a high lead site but no increase at a low lead site. Baes and Ragsdale
(1981) found significant post-1930 increases in oak (Quercus) and hickory (Carya) with high
lead exposure, but only In hickory with low lead exposure.
Pond sediment analyses (Shirahata, et al. 1980) have shown a 20-fold increase in lead
deposition during the last 150 years (Figure 5-1), documenting not only the increasing use of
lead since the beginning of the industrial revolution in western United States, but also the
relative fraction of natural vs. anthropogenic lead inputs. Other studies have shown the same
magnitude of increasing deposition in freshwater sediments (Chrlstensen and Chien, 1981;
Galloway and Likens, 1979; Edgington and Robbins, 1976), and marine sediments (Ng and
Patterson, 1982). The pond and marine sediments also document the shift in isotopic
composition caused by the recent opening of the New Lead Belt in Missouri, where the ore body
has an isotoplc composition substantially different from other ore bodies of the world.
Perhaps the best and certairrly the most controversial chronological record 1s that of the
polar fee strata of Murozuml et al. (1969), which extends nearly three thousand years back in
time (Figure 5-1). The data of Jaworowski et al. (1981) and Herron et al. (1977) do not agree
with the value found by Murozuml et al. (1969) for the early period around 800 B.C. Ng and
Patterson (1981) have shown that the ice cores of Herron et al. (1977) were contaminated with
023PB5/A
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PRELIMINARY DRAFT
1.0
0J
OJ
0.7
OJ
0.8
OJ
0.3
OJ
0.1
1760
1800
1826
1860
1900
1826
I860
1876
YEAR
Figure 5-1, Chronological record of the relative Increase of toad in snow strata, pond
and lake sediments, marina sadlments, and tree rings. The data are expressed as a
ratio of the latest year of the record and should not be interpreted to extend back in
time to natural or uncontamlnated levels of lead concentration.
Source: Adapted from Murozumi at al. (1969) (O), Shirahata at al. (1900) (~), Edgington
and Robbins (1978) (A), Ny and Patterson (1979) (A), and Roffe (1974) (•).
023PB5/A
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PRELIMINARY, ORAPT
industrial greases. Patterson (1983) has also discussed the probable errors .made by
Jaworowski et al. (1981) in their determination of manmade lead in glacial ice samples. At
the South Pole, Boutron (1982) observed a 4-fold increase of lead in snow from 1957 to 1977
but saw no increase during the period 1927 to 1957. The observed increase was attributed to
global rather than local or regional pollution. The author suggested the extensive
atmospheric lead pollution which began in the 1920's did not reach the South Pole until the
mid-1950's. This interpretation agrees with that of Maenhaut et al. (1979), who found
atmospheric concentrations of lead of 0.000076 pg/m3 at the same location. This concentration
is about 3-fold higher than the 0.000024 pg/m3 estimated by Patterson (1980) and Servant
(1982) to be the natural lead concentration in the atmosphere. In summary, it is likely that
atmospheric lead emissions have increased 2000-fold since the pre-Roman era, that even at this
early time the atmosphere may have been contaminated by a factor of three over natural levels
(Murozumi et al. 1969), and that global atmospheric concentrations have increased dramatically
since the 1920's.
The history of global emissions may also be determined from total production of lead, if
the fraction of that lead released to the atmosphere during the smelting process, the fraction
released during industrial consumption and the amount of lead emitted from non-lead sources
are known. The historical picture of lead production has been pieced together from many
sources by Settle and Patterson (1980) (Figure 5-2). They used records of accumulated silver
stocks to estimate the lead production needed to support coin production. Until the
industrial revolution, lead production was determined largely by the ability or desire to mine
lead for its silver content. Since that time, lead has been used as an industrial product in
its own right, and efforts to improve smelter efficiency, including control of stack emissions
and fugitive dusts, have made lead production more economical. This improved efficiency is
not reflected in the chronological record because of atmospheric emissions of lead from many
other anthropogenic sources, especially gasoline combustion (see Section 5.3.3). From this
knowledge of the chronological record, it is possible to sort out contemporary anthropogenic
emissions from natural sources of atmospheric lead.
5.2 NATURAL SOURCES
Lead enters the biosphere from lead-bearing minerals in the lithosphere through both
natural and man-made processes. Measurements of soil materials taken at 20-cm depths in the
continental United States (Lovering, 1976; Shacklette et al. 1971) show a median lead
concentration of 15 to 16 pg Pb/g soil. Ninety-five percent of these measurements show 30
pg/g of lead or less, with a maximum sample concentration of 700 pg/g.
023P85/A
5-3
7/13/83
-------
10*
10*
II?
g
$ 10*
Q
u
CC
i
z 10»
0
1
o w
£
101
10*
5600 5000 4600 4000 3600 3000 2600 2000 1600 1000 600 0
YEARS BEFORE PRESENT
Figure 5-2. The global lead production has changed historically in response to
major economic and political events. Increases in lead production (note log
scale) correspond approximately to historical increases in lead emissions shown
In Figure 5-1.
Source: Adapted from Settle and Patterson (1980).
In natural processes, lead is first incorporated in soil in the active root zone, from
which it may be absorbed by plants, leached into surface waters, or eroded into windborne
dusts (National Academy of Sciences, 1980; Chamberlain, 1970; Patterson, 1965; Chow and
Patterson, 1962).
Natural emissions of lead from volcanoes have been estimated by Nriagu (1979) to be 6400
t/year based on enrichment over crustal abundance. That is, 10 X 109 kg/year of volcanic dust
are produced, with an average concentration of 640 mq/9» or 40 times the crustal abundance of
16 pg/g. The enrichment factor is based on Lepel et al. (1978), who measured lead in the
PRELIMINARY DRAFT
8PANI8H PRODUCTION
OF SILVER J
IN NEW WORLD /
INDUSTRIAL
REVOLUTION
SILVER
PRODUCTION
IN GERMANY
EXHAUSTION
OF ROMAN
LEAD MINE8
INTRODUCTION
OF COINAGE
DISCOVERY OF
CUPELLATION
ROMAN REPUBLIC
AND EMPIRE
RISE AND FALL
OF ATHENS
023PB5/A
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plume Of the Augustine volcano in Alaska. Settle and Patterson (1980) have calculated
emissions of only i t/year, based on a measured Pb/S ratio of 1 X 10 7 and estimated sulfur
emissions of 6 X 10 t/year. This measured Pb/S ratio was from volcanoes reported by
Buat-Menard and Arnold (1978), and is likely to be a better estimate of lead emissions from
volcanoes.
Calculations of natural contributions using geochemical information indicate that natural
sources contribute a relatively small amount of lead to the atmosphere. For example, if the
typical 25 to 40 Mfl/m3 of rural airborne particulate matter consisted solely of wind-entrained
soils containing 15 fjg/g, and rarely more than 30 Mfl of lead/g, as cited above, then the
natural contribution to airborne lead would range from 0.0004 to 0.0012 yg/m3. It has been
estimated from geochemical evidence that the natural particulate lead level is less than
0.0005 (jg/m3 (National Academy of Sciences, 1980; United Kingdom Department of the
Environment, 1974). In fact, levels as low as 0.000076 vg/n3 have been measured at the South
Pole in Anarctica (Maenhaut et al., 1979). In contrast, average lead concentrations in urban
suspended particulate matter range as high as 6 yg/«i3 (Akland, 1976; U.S. Environmental
Protection Agency, 1979, 1978). Evidently, most of this urban particulate lead stems from
man-made sources.
5.3 MANNADE SOURCES
5.3.1 Production
Lead occupies an important position in the U.S. economy, ranking fifth among all metals
in tonnage used. Approximately 85 percent of the primary lead produced in this country is
from native mines, although often associated with minor amounts of zinc, cadmium, copper,
bismuth, gold, silver, and other minerals (U.S. Bureau of Mines, 1975). Missouri lead ore
deposits account for approximately 80 to 90 percent of the domestic production. Approximately
40 to 50 percent of annual lead production is recovered and eventually recycled.
5.3.2 Utilization
The 1971-1980 uses of lead are listed by major product category in Table 5-1 (U.S. Bureau
of Mines, 1972-1982). Total utilization averaged approximately 1.36x10® t/yr over the 10-year
period, with storage batteries and1 gasoline additives accounting for -70 percent of total use.
The gasoline antiknocks listed in Table 5-1 include additives for both domestic and import
markets. The additive fraction of total lead utilization has decreased from greater than 18
percent in 1971-1973 to less than 9.5 percent in 1981. Certain products, especially
batteries, cables, plumbing, weights, and ballast, contain lead that is economically
recoverable as secondary lead. This reserve of lead in use is estimated at 3.8 million metric
-------
TABLE 5-1. U.S. UTILIZATION OF LEAD BY MHJOUCT CATEGORY (1971-1981), METRIC TONS/YEAR
(U.S. BUREAU OF MINES, 1981, 1962)
Product category
1971
1972
1973
1974
1975
1976
1977
1978
1979
1980
1981
Storage batteries
tit,581
661,740
697,888
772,656
634,368
746,085
858,099
879,274
814,332
645,357
770,152
Gasoline antiknock
additive*
239,666
252,545
248,890
227,847
• 189,369
217,508
211,296
178,473
186,945
127,903
111,367
Pl^ents and ceraaics
73,701
80,917
98,651
105,405
71,718
95,792
90,704
91,642
90,790
78,430
80,165
¦**>
Aaaunitlon
79,423
76,822
73,091
78,991
68,098
66,659
62,043
55,776
53,236
48,662
49,514
so
m
rr
Solder
63,502
64,659
65,095
60,116
52,011
57,448
58,320
68,390
54,278
41,366
29,705
*-«
*
~—4
Cable covering!
47,998
41,659
39,006
39,387
20,044
14,452
13,705
13,851
16,393
13,408
12,072
|
o
g
Caulking lead
27,204
20,332
18,192
17,903
12,966
11,317
8,725
9,909
8,017
5,684
5,522
Pipe and sheet lead
41,523
37.592
40,529
34,238
35,456
34,680
30,861
23,105
27,618
28,393
28,184
Type Mtal
18,876
18,089
19,883
18,608
14,703
13,614
11,395
10,795
10,019
8,997
7,838
n
—1
Brass and bronze
18,180
17,963
20,621
20,172
12,157
14,207
15,148
16,502
18,748
13,Ml
13,306
Bearing ntili
14,771
14,435
14,201
13,250
11,051
11,851
10,873
9,510
9,630
7,808
6,922
Other
58,958
63,124
61,019
62,106
54,524
68,181
64,328
75,517
68,329
50,314
52,354
TOTAL '
1,298,383
1,349.846
1,397,876
1,450,679
1,176,465
1,351,794
1,435,497
1,432,744
1,358,335
1,070,303
1,167,101
•includes additives for both doaestic and export Barkets.
1
-------
PRELIMINARY DRAFT
tons, of which only 0.5 to 0.8 million metric tons are recovered annually. Lead in pigments,
gasoline additives, ammunition, foil, solder, and steel products is widely dispersed and
therefore is largely unrecoverable.
5.3.3 Emissions
Lead or its compounds may enter the environment at any point during mining, smelting,
processing, use, recycling, or disposal. Estimates of the dispersal of lead emissions into
the environment by principal sources indicate that the atmosphere is the major Initial
recipient. Estimated lead emissions to the atmosphere are shown in Table 5-2. Mobile and
stationary sources of lead emissions, although found throughout the nation, tend to be
concentrated in areas of high population density, with the exception of smelters. Figure 5-3
shows the approximate locations of major lead mines, primary and secondary smelters and
refineries, and alkyl lead plants (International Lead Zinc Research Organization, 1982).
5.3.3.1 Mobile Sources. The majority of lead compounds found in the atmosphere result from
leaded gasoline combustion. Several reports indicate that transportation sources, which
include light-duty, heavy-duty, and off-highway vehicles, contribute over 80 percent of the
total atmospheric lead (Nationwide [lead] emissions report, 1980, 1979; U.S. Environmental
Protection Agency, 1977). Other mobile sources, Including aviation use of leaded gasoline and
diesel and jet fuel combustion, contribute insignificant lead emissions to the atmosphere.
The detailed emissions inventory in Table 5-2 shows that 86 percent of the lead emissions in
the United States are from gasoline combustion. Cass and McRae (1983) assembled emissions
inventory data on the Los Angeles Basin and determined that 83 percent of the fine particle
emissions originated from highway vehicles. Lead is added to gasoline as an antiknock
additive to enhance engine performance in the form of two tetralkyl lead compounds, tetraethyl
and tetramethyl lead (see Section 3.4). Lead is emitted from vehicles primarily in the form
of inorganic particles, although a very small fraction (<10 percent) of lead emissions are
released as volatile organic compounds, i.e., lead alkyIs (National Academy of Sciences,
1972).
The factors which affect both the rate of particulate lead emissions and the
physicochemical properties of the emissions are: lead content of the fuel, other additives,
vehicle fuel economy, the driving speed or conditions, and type of vehicle, as well as design
parameters, maintenance, ages of the engine, exhaust, and emission control systems. The major
types of vehicles are light-duty (predominantly cars) and heavy-duty (trucks and buses). The
important properties of the particulate emissions Include the total amount emitted, the size
distribution of the particles, and the chemical composition of these particles as a function
of particle size. The most commonly used index of particle size is the mass median equivalent
023PB5/A
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PRELIMINARY DRAFT
TABLE 5-2. ESTIMATED ATMOSPHERIC LEAD EMISSIONS FOR THE
UNITED STATES, 1981, AND THE WORLD
Annual
Percentage of
Annual
U.S.
U.S. total
global
Source category
emissions
emissions
emissions
(t/yr)
(t/yr)
Gasoline combustion
35,000
85.9%
273,000
Waste oil combustion
830
2.0
8,900
Solid waste disposal
319
0.8
Coal combustion
950
2.3
14,000
Oil combustion
226
0.6
6,000
Wood combustion
—
—
4,500
Gray iron production
Iron and steel production
Secondary lead smelting
Primary copper smelting
Ore crushing and grinding
Primary lead smelting
Other metallurgical
Zn smelting
Ni smelting
Lead alfcyl manufacture
Type metal
Portland cement production
Miscellaneous
Total
295
533
631
30
326
921
54
245
85
71
233
40,739
0.7
1.3
1.5
0.1
0.8
2.3
0.1
0.6
0.2
0.2
0.5
100X
50,000
770
27,000
8,200
31,000
16,000
2,500
7,400
5,900
449,170
Inventory does not include emissions from exhausting workroom air, burning of lead-painted
surfaces, welding of lead-painted steel structures, or weathering of painted surfaces.
Source: For U.S. emissions, Battye (1983), for global emissions, Nriagu (1979).
023PB5/A
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o
rvj
w
¦o
CD
U1
ui
I
u>
-•J
o
00
¦ MINES (in
~ SMELTERS AND REFINERIES (7) '
O SECONDARY SMELTERS AND REFINERIES (66)
• LEAD ALKYL PLANTS (4)
Figure M. Locations of major lead operations in the United States.
Source: International Lead Zinc Research Organization (1982).
£
3D
•<
2
-------
PRELIMINARY DRAFT
diameter (MMED), which is defined as the point in the size distribution of particles such that
half the mass lies on either side of the WED value (National Air Pollution Control Adminis-
tration, 1970). Table 5-3 summarizes a recent study estimating the particulate emission rates
and particle composition for light-duty vehicles operated on a leaded fuel of 1.8 g Pb/galIon
(Hare and Black, 1981). Table 5-4 estimates particulate emission rates for heavy-duty
vehicles (trucks) operated on a leaded fuel of 1.8 g Pb/gal Ion (Hare and Black, 1981). The
lead content of 1.8 g Pb/gal1 on was chosen to approximate the lead concentration of leaded
gasoline during 1979 (Table 5-5). Another recent study utilizing similar composite emission
factors provides estimates of motor vehicle lead emissions for large areas (Provenzano, 1978).
lead occurs, on the average, as PbBrCl in fresh exhaust particles (Hirschler et al.,
1957). This lead compound is 64.2 percent lead by mass and is a common form of lead emitted
due to the presence of the scavengers ethylene dichloride and ethylene dibromide in normal
leaded fuel. PbBrCl has theoretical mass ratios for lead, bromine, and chlorine of 0.64,
0.25, and 0.11, respectively. The particle compositional data in Table 5-3 indicate that mass
ratios for lead, bromine, and chlorine are approximately 0.60, 0.30, and 0.10, respectively,
from both pre- and post-1970 vehicles. Data from another study (Lang et al., 1981), involving
1970-1979 vehicles, indicated that mass ratios for lead, bromine, and chlorine were 0.62,
0.30, and 0.08, respectively.
The fate of emitted lead particles depends upon their particle size (see Section 6.3.1).
Particles initially formed by condensation of lead compounds in the combustion gases are quite
small (well under 0.1 pm in diameter) (Pierson and Brachaczek, 1982). Particles in this size
category are subject to growth by coagulation and, when airborne, can remain suspended in the
atmosphere for 7 to 30 days and travel thousands of miles from their original source
(Chamberlain et al., 1979). Larger particles are formed as the result of agglomeration of
smaller condensation particles and have limited atmospheric lifetimes (Harrison and Laxen,
1981). The largest vehicle-emitted particles, which are greater than 100 pm in diameter, may
be formed by materials flaking off from the surfaces of the exhaust system. As Indicated in
Table 5-3, the estimated mass median equivalent diameter of leaded particles from light-duty
vehicles is <0,25 pm, suggesting that such particles have relatively long atmospheric
lifetimes and the potential for long-distance transport. Similar values for HHED in
automobile exhausts were found in Britain (0.27 pm) (Chamberlain et al. 1979) and Italy (0.33
pm) (Facchetti and Geiss, 1982). Particles this small deposit by Brownian diffusion and are
generally independent of gravitation.
The size distribution of lead exhaust particles 1s essentially bimodal (Pierson and
Brachaczek, 1976) and depends on a number of factors, including the particular driving pattern
1n which the vehicle is used and its past driving history (Ganley and Springer, 1974; Habibi,
023PB5/A
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PRELIMINARY DRAFT
TABLE 5-3. LIGHT-DUTY VEHICULAR PARTICULATE EMISSIONS*
Data by vehicle category
1970 & later
Rate or property
Pre-1970
without catalyst
Exhaust particulate emissions, g/mi
0.29
0.13
Particle mass aedian equivalent diameter, (jn
<0.25
<0.25
Percent of particulate mass as:
Lead (Pb)
22 or greater
36 or greater
Bromine (Br)
11 or greater
18 or greater
Chlorine (CI)
4 or greater
6 or greater
Trace metals
1
1 or greater
Carbon (C), total
33 or greater
33 or less
Sulfate (S04")
1.3
1.3 or greater
Soluble organics
~30 or less
~10
*Rate estimates are based on 1.8 Pb/gal fuel.
Source: Hare and Black (1981).
TABLE 5-4. HEAVY-DUTY VEHICULAR PARTICULATE EMISSIONS*
Particulate eMissions by model year
Heavy-duty category Pre-1970 1970 and later
Medium-duty trucks 0.50 0.40
(6,000 to 10,000 lb GVW)
Heavy-duty trucks 0.76 0.60
(over 10,000 lb GVW)
*Rate estimates are based on 1.8 g Pb/gal fuel, units are g/mi.
Source: Hare and Black (1981).
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PRELIMINARY DRAFT
TABLE 5-5. RECENT AND PROJECTED CONSUMPTION OF GASOLINE LEAD
Average lead content
dj7giTf
Sales Total lead Air-lead
1 ' 1 '3
Gasoline voluwe weighted (103t) (pfl/m3)
Calendar (billions of gallons) total 0.5 gpg 1.1 gpg
year Total Leaded pool Leaded pooled std leaded std
1975
102.3
92.5
1.62
1.81
165.6
—
1.23
1976
107.0
87.0
1.60
1.97
171.0
—
1.22
1977
113.2
79.7
1.49
2.12
168.7
—
1.20
1978
115.8
75.0
1.32
2.04
153.3
—
1.13
1979
111.2
68.1
1.16
1.90
129.5
—
0.93
1980
110.8
57.5
0.71
1.37
78.5
—
0.60
1981
102.6
51.0
0.59
1.19
61.0
—
0.47^
1982
100.0
40.6
0.64
1.44
62.0
———
0.45
1983b
96.1
41.7
48.1
47.0
1984
92.3
35.4
0.50
1.10
46.1
39.0
1985
89.2
29.7
0.50
1.10
44.6
32.7
1986
86.1
25.3
0.50
1.10
43.0
27.8
1987
83.8
22.1
0.50
1.10
41.9
24.3
1988
81.5
19.5
0.50
1.10
40.7
21.4
1989
79.2
17.0
0.50
1.10
39.6
18.7
1990
77.7
14.7
0.50
1.10
38.8
16.2
Data for the years 1975-1982 are taken fro# U.S. Environmental Protection Agency
(1983b), in which data for 1975-1981 are actual consumption of lead and for 1982,
estimates of consumption.
''Data for 1983-1990 are estimates taken from F.R. (1982 October 29).
cEst1mated (this work)
dData from Hunt and Neligan (1982), discussed in Chapter 7, are the maximum
quarterly average lead levels from a composite of sampling sites.
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PRELIMINARY DRAFT
1973; 1970; Ter Haar et al., 1972; Hirschler and Gilbert, 1964; Hirschler et al., 1957). As
an overall average, it has been estimated that during the lifetime of the vehicle,
approximately 35 percent of the lead contained in the gasoline burned by the vehicle will be
emitted as small particles (<0.25 MMED), and approximately 40 percent will be emitted as
larger particles (>10 m« MMED) (Ter Haar et al., 1972). The remainder of the lead consumed in
gasoline combustion is deposited in the engine and exhaust system. Engine deposits are, in
part, gradually transferred to the lubricating oil and removed from the vehicle when the oil
is changed. A flow chart depicting lead-only emissions per gallon of fuel charged into the
engine is shown in Figure 5-4. It is estimated that 10 percent of the lead consumed during
combustion is released into the environment via disposal of used lubricating oil (Piver,
1977). In addition, some of the lead deposited in the exhaust system gradually flakes off, is
emitted in the exhaust as extremely large particles, and rapidly falls into the streets and
roads where it is Incorporated into the dust and washed into sewers or onto adjacent soil.
Although the majority (>90 percent on a mass basis) of vehicular lead compounds are
emitted as inorganic particles (e.g., PbBrCl), some organolead vapors (e.g., lead alkyls) are
also emitted. The largest volume of organolead vapors arises from the manufacture, transport,
and handling of leaded gasoline. Such vapors are photoreactive, and their presence in local
atmospheres is transitory, i.e., the estimated atmospheric half-Hves of lead alkyls, under
typical summertime conditions, are less than half a day (Nielsen, 1982). Organolead vapors
are most likely to occur in occupational settings (e.g., gasoline transport and handling
operations, gas stations, parking garages) and have been found to contribute less than 10
percent of the total lead present in the atmosphere (Gibson and Farmer, 1981; National Academy
of Sciences, 1972).
The use of lead additives in gasoline, which increased in volume for many years, is now
decreasing as automobiles designed to use unleaded fuel constitute the major portion of the
automotive population (Table 5-1). The decline in the use of leaded fuel is the result of two
regulations promulgated by the U.S. Environmental Protection Agency (F.R., 1973 December 6).
The first required the availability of unleaded fuel for use in automobiles designed to meet
federal emission standards with lead-sensitive emission control devices (e.g., catalytic
converters); the second required a reduction or phase-down of the lead content in leaded
gasoline. Compliance with the phase-down of lead in gasoline has recently been the subject of
proposed rulemakings. The final action (F.R., 1982 October 29) replaced the present 0.5 g/gal
standard for the average lead content of all gasoline with a two-tiered standard for the lead
content of leaded gasoline. Under this proposed rule, large refineries would be required to
meet a standard of 1.10 g/gal for leaded gasoline while certain small refiners would be
subject to a 1.90 g/gal standard until July 1, 1983, at which time they were made subject to
the 1.10 g/gal standard.
023PB5/A 5-13 7/13/83
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-V3B*
LEADED FUEL ^
(Pb - IjO rtpti^
WOO mg (WOW-
TOTAL MA88 OF LEAD
CHARGED INTO THE
ENGINE
AUTO 1 »
ENGINE TAILPIPE DEPOSfTION ^ 1B* /,
'VIO*
1B0 mg-RETAINED ON
INTERIOR SURFACES OF
BMMNE AND EXHAUST
SYSTEM
-\*o%
m' 360 mg Pb EMITTED SS
&S TO ATM08PHERE AS ^
P LEAD AEROSOL WITH 'i
MASS MEDIAN DIAMETER
OF <0.26 nm. POTENTIAL:
FOR LONG RANGE J
I TRANSPORT/POLLUTION. :
f 400rog rt EMITtiib To i
! ROADWAY AS PARTICLES
ifc WITH MASS MEDIAN
8? DIAMETERS >10 |iin %
£ LOCALIZED POLLUTION. V
100 mg Pb RETAINED BY
LUBRICATING OIL
EXHAUST PRODUCTS
^78% (7B0 mg TOTAL
Pb EMITTED)
Figure 5-4. Estimated lead-only emissions distribution per gallon of combusted fuel.
-------
PRELIMINARY DRAFT
The trend in lead content for U.S. gasolines is shown in Figure 5-5 and Table 5-5. Of
the total gasoline pool, which includes both leaded and unleaded fuels, the average lead
content has decreased 63 percent, from an average of 1.62 g/gal in 1975 to 0.60 g/gal in 1981
(Table 5-5, Figure 5-5). Accompanying the phase-down of lead in leaded fuel has been the
increased consumption of unleaded fuel, from 11 percent of the total gasoline pool in 1975 to
50 percent in 1981 (Table 5-5 and Figure 5-6). Since 1975, when the catalytic converter was
introduced by automobile manufacturers for automotive exhaust emissions control, virtually all
new passenger cars have been certified on unleaded gasoline (with the exception of a few
diesels and a very few leaded-gasoline vehicles). Because of the yearly turnover rate in the
vehicle fleet, the demand for unleaded gasoline 1s forecast to Increase to 58 percent of the
total gasoline pool in 1982 and ~75 percent by 1985. As the demand for unleaded fuel
increases, it may become uneconomical to distribute leaded gasoline for light-duty vehicles 1n
low-volume localities.
The lead content of leaded gasoline (Table 5-5) is forecast to increase from 1.19 to^l.44
g/gal in 1982 (DuPont de Nemours, 1982). The reason for this increase is that under the 1982
0.5 g/gal total pool standard, refiners could add ever-increasing amounts of lead to each
gallon of leaded gasoline (up to the level at which it would no longer be economically
justified) as the amount of unleaded gasoline produced by the refinery increases. Thus, as
the amount of unleaded gasoline increased, the amount of lead in leaded gasoline could also
Increase under the former regulations. The recent EPA decision (F.R., 1982 October 29)
eliminated this practice, thereby ensuring that the amount of lead used in gasoline will
decline after 1982 to 1.1 g/gal. Further decreases in lead emissions from gasoline combustion
will depend on continued reductions in the sales of leaded gasoline.
Data describing the lead consumed in gasoline and average ambient lead levels (composite
of maximum quarterly values) versus calendar year are listed in Table 5-5 and plotted 1n
Figure 5-7. The 1975 through 1979 composite quarterly lead averages are based on 105
lead-monitoring sites, primarily urban. The 1980 composite average 1s based on 58 sites with
valid annual data. The EPA National Aerometric Data Base is still receiving the 1980 data.
The linear correlation (Figure 5-8) between lead consumed in gasoline and the composite
maximum average quarterly ambient average lead level is very good with r2 = 0.99. The 1981
and 1982 composite averages shown in Table 5-5 and Figures 5-7 and 5-8 are derived using the
linear equation of Figure 5-6. Between 1975 and 1980, the lead consumed in gasoline decreased
52 percent (from 165,577 metric tons to 78,679 metric tons) while the corresponding composite
maximum quarterly average of ambient lead decreased 51 percent (from 1.23 pg/m3 to 0.60
pg/m3). This Indicates that control of lead in gasoline over the past several years has
effected a direct decrease 1n peak ambient lead concentrations, at least for this group of
monitoring sites.
023PB5/A 5-15 7/13/83 ^
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2.40
PRELIMINARY DRAFT
! ^
2.00
LEADED FUEL
1
g
Z
~
O
3
u.
O
H
8
ui
1.60
1.00
8ALES-WEIG HTED TOTAL
QASOUNiPOOL
(LEADED AND UNLEADED
"AVERAGE"!
0.B0 -
0.00
UNLEADED FUEL
+ t t
1 *
1t7B
1976
1977
1161
it82*
im 1970 1980
CALENDAR YEAR
Figure 5-5. Trend in lead content of U.S. gasolines, 1975-1982. (DuPont, 1982).
•1982 OATA ARE FORECASTS.
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120
110
100
90
80
70
80
80
40
30
20
10
0
PRELIMINARY DRAFT
TOTAL GASOLINE SALES
UNLEADED
EGULAR
LEADED
, 1-
'itk t,-
¦ uw
LEADED premium
187B
1978
1981 1982*
CALENDAR YEAR
Figure 6-6. Trend in U.S. gasoline sales, 1975-1982. (DuPont, 1962).
*1982 DATA ARE FORECASTS.
5-17
7/01/8'
-------
% %
200
180 - 200
180
ut 140
Z
~
O
O
ui
120
1 100
Z
o
o
o
§ 80
60
40
20
180
160
140
120
100
80
80
40
20
AMBIENT liAD CONCENTRATION
LEAD CON8UMIO IN OASOUNE
1J0
1.10 8
z
1.00
0J0
0.80
0.70
0.60
OJO
0.40
0.30
1871 1976 1877 1878 1878 1880 1881# 1882«
CALENDAR YEAR
Figure 5-7. Lead consumed in gasoline (Du Pont, 1982) and ambient lead con-
centrations, 1976-1982. (Hunt and Neligan, 1982).
•DASHED LINES ARE ESTIMATES.
5"18 7/01/83
-------
AVERAGE Pb - 6.93 x 10* CPb CONSUMED) + 0.06
,•1980
0.20 0.40 0.60 0.80 1.00 1.20
COMPOSITE MAXIMUM QUARTERLY AVERAGE LEAD LEVELS, HO'm*
Figure 5-8. Relationship between lead consumed in gasoline and composite maximum
quarterly average lead level*. 1976-1980.
•1981 AND 1982 DATA ARE ESTIMATES.
5-19
7/01/83
-------
PRELIMINARY DRAFT
Furthermore, the equation in Figure 5-8 implies that the complete elimination of lead
from gasoline might reduce the composite average of the maximum quarterly lead concentrations
at these stations to 0.05 mq/"3» a level typical of concentrations reported for nonurban
stations in the U.S. (see Chapter 7). Even this level of 0.05 pg/m3 is regarded as evidence
of human activity since it is at least two orders of magnitude higher than estimates of
geochemical background lead concentrations discussed in Section 5.2.
5.3.3.2 Stationary Sources. As shown in Table 5-2 (based on 1982 emission estimates), solid
waste incineration and combustion of waste oil are the principal contributors of lead
emissions from stationary sources, accounting for two-thirds of stationary source emissions.
The manufacture of consumer products such as lead glass, storage batteries, and lead additives
for gasoline also contributes significantly to stationary source lead emissions. Since 1970,
the quantity of lead emitted from the metallurgical industry has decreased somewhat because of
the application of control equipment and the closing of several plants, particularly in the
zinc and pyrometallurgical industries.
A new locus for lead emissions emerged in the mid-1960s with the opening of the "Viburnum
Trend" or "New Lead Belt" in southeastern Missouri. The presence of ten mines and three
accompanying lead smelters in this area makes it the largest lead-producing district in the
world and has moved the United States into first place among the world's lead-producing
nations.
Although some contamination of soil and water occurs as a result of such mechanisms as
leaching from mine and smelter wastes, quantitative estimates of the extent of this
contamination are not available. Spillage of ore concentrates from open trucks and railroad
cars, however, is known to contribute significantly to contamination along transportation
routes. For example, along two routes used by ore trucks in southeastern Missouri, lead
levels in leaf litter ranged from 2000 to 5000 pg/g at the roadway, declining to a fairly
constant 100 to 200 yq/q beyond about 400 ft from the roadway (Wixson et al., 1977).
Another possible source of land or water contamination 1s the disposal of particulate
lead collected by air pollution control systems. The potential impact on soil and water
systems from the disposal of dusts collected by these control systems has not been quantified.
5.4 SUMMARY
There is no doubt that atmospheric lead has been a component of the human environment
since the earliest written record of civilization. Atmospheric emissions are recorded in
glacial ice strata and pond and lake sediments. The history of these global emissions seems
closely tied to production of lead by industrially oriented civilizations.
023PB5/A
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PRELIMINARY DRAFT
Although the amount of lead em'tted from natural sources 1s a subject of controversy,
even the most liberal estimate (25 X 103 t/year) is dwarfed by the global emissions from
anthropogenic sources (450 X 103 t/year).
Production of lead in the United States has remained steady at about 1.2 X 10® t/year for
the past decade. The gasoline additive share of this market has dropped fro# 18 to 9.5
percent during the period 1971 to 1981. The contribution of gasoline lead to total
atmospheric emissions has regained high, at 85 percent, as emissions from stationary sources
have decreased at the sane pace as from mobile sources. The decrease in stationary source
emissions is due primarily to control of stack emissions, whereas the decrease in mobile
source emissions is a result of switchover to unleaded gasolines. The decreasing use of lead
in gasoline is projected to continue through 1990.
023PB5/A
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PRELIMINARY DRAFT
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6. TRANSPORT AND TRANSFORMATION
6.1 INTRODUCTION
This chapter describes the transition from the emission of lead particles Into the
atmosphere to their ultimate deposition on environmental surfaces, i.e., vegetation, soli, or
water. At the source, lead emissions are typically around 10,000 \tg/ma (see Section 5.3.3),
while in city air, lead values are usually between 0.1 and 10 MS/™3 (Dzubay et al., 1979;
Reiter et al., 1977; also see Chapter 7). These reduced concentrations are the result of
dilution of effluent gas with clean air and the removal of particles by wet or dry deposition.
Characteristically, lead concentrations are highest in confined areas close to sources and are
progressively reduced by dilution or deposition in districts more removed from sources.
At any particular location and time, the concentration of lead found in the atmosphere
depends on the proximity to the source, the amount of lead emitted from sources, and the
degree of mixing provided by the motion of the atmosphere. It is possible to describe
quantitatively the physics of atmospheric mixing in a variety of ways and, with some limiting
assumptions, to develop simulation models that predict atmospheric lead concentrations. These
models are not sensitive to short-term variations in air motion over a period of weeks or
months because these variations are suppressed by integration over long periods of time.
In highly confined areas such as parking garages or tunnels, atmospheric lead
concentrations can be ten to a thousand tines greater than values measured near roadways or in
urban areas. In turn, atmospheric lead concentrations are usually about 2% times greater in
the central city than in residential suburbs. Rural areas have even lower concentrations.
Because lead emissions in the United States have declined dramatically in the past few
years, the older lead concentration data on which recent dispersion studies are based may seem
not to be pertinent to existing conditions. Such studies do in fact illustrate principles of
atmospheric dispersion and may validly be applied to existing concentrations of lead, which
are described in Section 7.2.1.1.
Transformations which may occur during dispersion are physical changes in particle size
distribution, chemical changes from the organic to the Inorganic phase, and chemical changes
in the inorganic phase of lead particles. Particle size distribution stabilizes within a few
hundred kilometers of the sources, although atmospheric concentration continues to decrease
with distance. Concentrations of organolead compounds are relatively small (1 to 6 percent of
total lead) except in special situations where gasoline is handled or where engines are
started cold within confined areas. Ambient organolead concentrations decrease more rapidly
than inorganic lead, suggesting conversion from the organic to the inorganic phase during
transport. Inorganic lead appears to convert from lead halides and oxides to lead sulfates.
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PRELIMINARY DRAFT
Lead is removed fro* the atmosphere by wet or dry deposition. The mechanisms of dry
deposition have been incorporated into models that estimate the flux of ataospherlc lead to
the Earth's surface. Of particular Interest is deposition on vegetation surfaces, since this
lead may be incorporated Into food chains. Between wet and dry deposition, it is possible to
calculate an atmospheric lead budget that balances the emission Inputs discussed in Section
5.3.3. with deposition outputs.
6.2 TRANSPORT OF LEAD IN AIR BY DISPERSION
6.2.1 Fluid Mechanics of Dispersion
Particles in air streams are subject to the same principles of fluid mechanics as
particles 1n flowing water (Friedlander, 1977). On this basis, the authors of several texts
have described the mathematical arguments for the mixing of polluted air with clean air
(Benarie, 1980; Dobbins, 1979; Pasquill, 1974). The first principle is that of diffusion
along a concentration gradient. If the airflow is steady and free of turbulence, the rate of
mixing is determined by the diffuslvity of the pollutant. In the case of gases, this
dlffusivlty is an inherent property of the molecular forces between gases. For particles,
diffusivlty is a property of Brownian movement, hence a function of particle size and
concentration. For both cases, the diffusivlty for dilute media 1s a constant (Dobbins,
1979).
If the steady flow of air 1s Interrupted by obstacles near the ground, turbulent eddies
or vortices may be formed. Diffusivlty is no longer constant but may be Influenced by factors
independent of concentrations, such as wlndspeed, atmospheric stability, and the nature of the
obstacle. By making generalizations of wlndspeed, stability, and surface roughness, it is
possible to construct models using a variable transport factor called eddy diffusivlty (K), in
which K varies 1n each direction, including vertically. There is a family of K-theory models
that describe the dispersion of particulate pollutants.
The simplest K-theory model assumes that the surface is uniform and the wind is steady;
thus, turbulence 1s predictable for various conditions of atmospheric stability (Pasquill,
1974). This model produces a Gaussian plume, called such because the concentration of the
pollutant decreases according to a normal or Gaussian distribution in both the vertical and
horizontal directions. These models have some utility and are the basis for most of the air
quality simulations performed to date (Benarie, 1980). However, the assumptions of steady
wlndspeed and smooth surface place constraints on their utility.
Several approaches have been used to circumvent the constraints of the Gaussian models.
Some have been adapted for studying long range transport (LRT) (more than 100 km) of
pollutants. Johnson (1981) discusses 35 LRT models developed during the 1970s to describe the
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PRELIMINARY DRAFT
dispersion of atmospheric sulfur compounds. A few models that address specific problems of
local and regional transport merit further discussion because they emphasize the scope of the
modeling problem.
One family of models is based on the conservative volume element approach, where volumes
of air are seen as discrete parcels having conservative meteorological properties, such as
water vapor mixing ratio, potential temperature, and absolute vorticity (Benarle, 1980). The
effect of pollutants on these parcels is expressed as a mixing ratio. These parcels of air
may be considered to move along a trajectory that follows the advective wind direction. These
models are particularly suitable for dealing with surface roughness, but they tend to
introduce artifact diffusion or pseudodiffusion, which must be suppressed by calculation (Egan
and Mahoney, 1972; Liu and Seinfeld, 1975; Long and Pepper, 1976).
An approach useful for estimating dispersion from a roadway derives from the similarity
approach of Prandtl (1927). A mixing length parameter is related to the distance traveled by
turbulent eddies during which violent exchange of material occurs. This mixing length is
mathematically related to the square root of the shear stress between the atmosphere and the
surface. Richardson and Procter (1925) formulated these concepts in a law of atmospheric
diffusion which was further extended to boundary layer concepts by Obukhov (1941). At the
boundary layer, the turbulent eddy grows and its energy decreases proportionately with time
and distance away from the source.
Although physical descriptions of turbulent diffusion exist for idealized circumstances
such as isolated roadways and flat terrain, the complex flow and turbulence patterns of cities
has defied theoretical description. The permeability of street patterns and turbulent eddy
development in street canyons are two major problem areas that make modeling urban atmospheres
difficult. Kotake and Sano (1981) have developed a simulation model for describing air flow
and pollutant dispersion in various combinations of streets and buildings on two scales. A
small scale, 2 to 20 m, is used to define the boundary conditions for 2 to 4 buildings and
associated roadways. These subprograms are combined on a large scale of 50 to 500 meters.
Simulations for oxides of nitrogen show nonlinear turbulent diffusion, as would be expected.
The primary utility of this program 1s to establish the limits of uncertainty, the first step
toward making firm predictions. It is likely that the development of more complete models of
dispersion in complex terrains will become a reality in the near future.
An important point in this discussion is that none of the models described above have
been tested for lead. The reason for this is simple. All of the models require sampling
periods of 2 hours or less in order for the sample to conform to a well-defined set ol
meteorological conditions. In most cases, such a sample would be below the detection limits
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for lead. The common pollutant used to test models is S02, which can be measured over very
short, nearly instantaneous, time periods. The question of whether gaseous S02 can be used as
a surrogate for particulate lead in these models remains to be answered.
6.2.2 Influence of Dispersion on Ambient Lead Concentrations
Dispersion within confined situations, such as parking garages, residential garages and
tunnels, and away from expressways and other roadways not influenced by complex terrain
features depends on emission rates and the volume of clean air available for mixing. These
factors are relatively easy to estimate and some effort has been made to describe ambient lead
concentrations which can result under selected conditions. On an urban scale, the routes of
transport are not clearly defined, but can be inferred from an isopleth, i.e., a plot
connecting points of identical ambient concentrations. These plots always show that lead
concentrations are maximum where traffic density is highest.
Dispersion beyond cities to regional and remote locations is complicated by the fact that
there are no monitoring network data from which to construct isopleths, that removal by
deposition plays a more important role with time and distance, and that emissions from many
different geographic location's sources converge. Some techniques of source reconciliation
are described, but these become less precise with increasing distance from major sources of
lead. Dispersion from point sources such as smelters and refineries is described with
isopleths in the manner of urban dispersion, although the available data are notably less
abundant.
6.2.2.1 Confined and Roadway Situations. Obviously, the more source emissions are diluted by
clean air, the lower ambient air concentrations of lead will be. Ingalls and Garbe (1982)
used a variety of box and Gaussian plume models to calculate typical levels of automotive air
pollutants that might be present in microscale (within 100 meters of the source) situations
with limited ventilation. Table 6-1 shows a comparison of six exposure situations, recomputed
for a flat-average lead emission factor of 6.3 mg/km for roadway situations and 1.0 mg/min for
garage situations. The roadway emission factor chosen corresponds roughly to values chosen by
Dzubay et al. (1979) and Pierson and Brachaczek (1976) scaled to 1979 lead-use statistics.
The parking garage factor was estimated from roadway factors by correction for fuel
consumption (Ingalls and Garbe, 1982).
Confined situations, with low air volumes and little ventilation, allow automotive
pollutant concentrations to reach one to three orders of magnitude higher than are found in
open air. Thus, parking garages and tunnels are likely to have considerably higher ambient
lead concentrations than are found in expressways with high traffic density or in city
streets. Purdue et al. (1973) found total lead levels of 1.4 to 2.3 pg/m3 1n five of six U.S.
cities in 1972. In similar samples from an underground parking garage, total lead was 11 to
12 pg/m8.
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PRELIMINARY DRAFT
Table 6-1 also shows that the high concentration of automotive lead near roadways
declines significantly at distances greater than 100 meters. Dzubay et al. (1979) found lead
concentrations of 4 to 20 Mg/rn3 in air over Los Angeles freeways in 1976; at nearby sites off
the freeways, concentrations of 0.3 to 4.7 jjg/m3 were measured.
TABLE 6-1. SUMMARY OF MICROSCALE CONCENTRATIONS
Data are recalculated from Ingalls and Garbe (1982) using 1979 lead emission factors. They
show that air lead concentrations in a garage or tunnel can be two or three orders of magni-
tude higher than on streets or expressways. Typical conditions refer to neutral atmospheric
stability and average dally traffic volumes. Severe conditions refer to maximum hourly
traffic volume with atmospheric inversion. Data are in jjg/m3. Emission rates are given in
parentheses.
Air lead
Situation concentration
Residential garage (1 Rig Pb/min)
Typical (30 second idle time)
Severe (5 min idle time)
Parking garage (1 mg Pb/min)
Typical
Severe
Roadway tunnel (6.3 mg Pb/km)
Typical
Severe
Street canyon (sidewalk receptor) (6.3 mg Pb/km)
Typical a) 800 vehicles/hr
b) 1,600 vehicles/hr
80
670
40
560
11
29
Severe a) 800 vehicles/hr
b) 1,600 vehicles/hr
1.4
2.8
On expressway (wind: 315 deg. rel.
Typical
Severe
Beside expressway (6.3 mg Pb/km)
Severe 1 meter
10 meters
100 meters
1,000 meters
1 m/sec) (6.3 mg Pb/km)
30 min
"1
6
2
0.25
2.
10
Annual
l.Q
0.3
0.03
average
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Tiao and H11liner (1978) and Ledolter and Tiao (1979) have analyzed 3 years (1974-1977) of
ambient air lead data fro* one site on the San Diego Freeway in Los Angeles, California.
Particulate lead concentrations were measured at five locations: in the median strip and at
distances of 8 and 30 to 35 meters fro# the road edge on both sides of the road. Average lead
concentrations at the 35 meter point were two- to four-fold lower than at the 8 meter location
(Tiao and Hillmer, 1978). An empirical model Involving traffic count and traffic speed, which
are related to road emissions, required only windspeed as a predictor of dispersion
conditions.
Witz et al. (1982) found that meteorological parameters in addition to windspeed, such as
inversion frequency, inversion duration, and temperature, correlate well with ambient levels
of lead. At a different site near the San Diego freeway in Los Angeles, monthly ambient
particulate lead concentrations and meteorological variables were measured about 100 meters
from the roadway through 1980. Multiple linear regression analysis showed that temperature at
6 AM, windspeed, wind direction, and a surface-based inversion factor were important variables
in accurately predicting monthly average lead concentrations. In this data set, lead values
for December were about five-fold higher than those measured in the May to September summer
season, suggesting that seasonal variations in wind direction and the occurrence of
surface-based inversions favor high winter lead values. Unusually high early morning
temperatures and windspeed during the winter increased dispersion and reduced lead
concentration. The success of this empirical model depends on the interplay of windspeed and
atmospheric stability (Witz et al., 1982).
6.2.2.2 Dispersion of Lead on an Urban Scale. In cities, air pollutants including lead that
are emitted from automobiles tend to be highest in concentration in high traffic areas. Most
U.S. cities have a well-defined central business district (CBD) where lead concentrations are
highest. To illustrate the dispersion of lead experienced in cities, two cases are presented
below.
Trijonis et al. (1980) reported lead concentrations for seven sites in St. Louis,
Missouri; annual averages for 1977 are shown in Figure 6-1. Values around the CBD are
typically two to three times greater than those found in the outlying suburbs in St. Louis
County to the west of the city. Bradow (1980) presented results from the Regional Air
Monitoring System Gaussian plume model (Turner, 1979) for St. Louis for the 1977 calendar
year. Figure 6-1 also presents isopleths for lead concentration calculated from that model.
The general picture is one of peak concentrations within congested commercial districts which
gradually decline 1n outlying areas. However, concentration gradients are not steep, and the
whole urban area has levels of lead above 0.5 pg/m8.
023PB6/A
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PRELIMINARY DRAFT
n. ^ 1 1 ¦
N.\ \ \ I
r-'j
N- s (
ST. CHARLES COUNTY, MO
82.(64
MADISON COUNTY, ILi
«M AAJ
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PRELIMINARY DRAFT
For the South Coast Basin of Southern California, the area of high traffic density is
more widespread than is characteristic of many cities. Ambient concentrations of lead tend to
be more uniform. For example. Figures 6-2 and 6-3 show the average daily traffic by grid
square and the contour plots of annual average lead concentration, respectively, for 1969
(Kawecki, 1978). In addition, Figure 6-3 shows annual average lead measured at eight sites in
the Basin for that year. It is clear that the central portion had atmospheric particulate
lead concentrations in the range of 3 pg/m3; the outer areas were about 1 to 2 pg/m3.
Reiter et all. (1977) have shown similar results for the town of Fort Collins, Colorado,
for a 5.5-hr period in Hay of 1973. In that study, modeling results showed maximum lead
concentrations in the center of town around 0.25 jjg/m8, which decreased to 0.1 (jg/nt3 in the
outermost region. Presumably, still lower values would be found at more remote locations.
Apparently, then, lead in the air decreases 2Vfold from maximum values in center city
areas to well populated suburbs, with a further 2-fold decrease in the outlying areas. These
modeling estimates are generally confirmed by measurement in the cases cited above and in the
data presented in Section 7.2.1.
6.2.2.3 Dispersion from Smelter and Refinery locations. The 15 mines and 7 primary smelters
and refineries shown in Figure 5-3 are not located in urban areas. Most of the 56 secondary
smelters and refineries are likewise non-urban. Consequently, dispersion from these point
sources should be considered separately, but in a manner similar to the treatment of urban
regions. In addition to lead concentrations in air, concentrations in soil and on vegetation
surfaces are often used to determine the extent of dispersion away from smelters and
refineries.
6.2.2.4 Dispersion to Regional and Remote Locations. Beyond the Immediate vicinity of urban
areas and smelter sites, lead in air declines rapidly to concentrations of 0.1 to 0.5 ytg/ttfi.
Two mechanisms responsible for this change are dilution with clean air and removal by
deposition (Section 6.4). In the absence of monitoring networks that might identify the
sources of lead in remote areas, two techniques of source Identification have been used.
Vector gradient analysis was attempted by Everett et al. (1979) and source reconciliation has
been reported by Sievering et al. (1980) and Cass and McRae (1983). A third technique, isoto-
pic composition, has been used to identify anthropogenic lead in air, sediments, soils,
plants, and animals in urban, rural, and remote locations (Chow et al. 1975), but this
technique is not discussed here because it provides no information on the mechanism of
transport.
023PB6/A
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PRELIMINARY DRAFT
342
710
1306
666
207
96
6
6
4
1
0
4
0
•37
1037
1612
1644
919
339
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143
4
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1
4
0
800
963
1671
2006
1607
•
Q
1669
692
.ENDA
^PASi
.1
1179
l|
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420
USA
266
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86
we
10
T LOS
1296
ANGEL
1324
:S
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T GOV
INA
hi
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.OS AR
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QELES
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2043
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1672 (
DX
ILYNW
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5
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946
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0
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-
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.199
0
Figure 6-2. Spatial distribution of surface street and freeway traffic In the Los
Angeles Basin (10* VMT/day) for 1979.
Source: Kawacki (1978).
023PB6/A
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PRELIMINARY DRAFT
1 »gJm'
3 nfl/m
Figure 6-3. Annual average suspended lead concentrations for 1969 in the Los
Angeles Basin, calculated from the model of Cass (1975). The white zones between
the patterned areas are transitional zones between the indicated concentrations.
Source: Kawecki (1978).
Q23PB6/A
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PRELIMINARY DRAFT
In vector gradient analysis, the sampler is oriented to the direction of the incoming
wind vector, and samples are taken only during the time the wind is within a 30° arc of that
vector. Other meteorological data are taken continuously. As the wind vector changes, a
different sampler is turned on. A 360° plot of concentration vs. wind direction gives the
direction from which the pollutant arrives at that location. Only one report of the use of
this technique for lead occurs in the literature (Everett et al., 1979), and analysis of this
experiment was complicated by the fact that in more than half the samples, the lead con-
centrations were below the detection limit. The study was conducted at Argonne National
Laboratory and the results reflected the influence of automobile traffic east and northeast of
this location.
Source reconciliation is based on the concept that each type of natural or anthropogenic
emission has a unique combination of elemental concentrations. Measurements of ambient air,
properly weighted during multivariate regression analysis, should reflect the relative amount
of pollutant derived from each of several sources (Stolzenberg et al., 1982). Sievering et
al. (1980) used the method of Stolzenberg et al. (1982) to analyze the transport of urban air
from Chicago over Lake Michigan. They found that 95 percent of the lead in Lake Michigan air
could be attributed to various anthropogenic sources, namely coal fly ash, cement manufacture,
iron and steel manufacture, agricultural soil dust, construction soil dust, and incineration
emissions. This information alone does not describe transport processes, but the study was
repeated for several locations to show the changing influence of each source.
Cass and McRae (1983) used source reconciliation in the Los Angeles Basin to interpret
1976 NFAN data (see Sections 4.2.1 and 7.2.1.1) based on emission profiles from several
sources. They developed a chemical element balance model, a chemical tracer model, and a
multivariate statistical model. The chemical element balance model showed that 20 to 22
percent of the total suspended particle mass could be attributed to highway sources. The
chemical tracer model permitted the lead concentration alone to represent the highway profile,
since lead comprised about 12 percent of the mass of the highway generated aerosol. The
multivariate statistical model used only air quality data without source emission profiles to
estimate stoichiometric coefficients of the model equation. The study showed that single
element concentrations can be used to predict the mass of total suspended particles.
A type of source reconciliation, chemical mass balance, has been used for many years
by geochemists in determining the anthropogenic influence on the global distribution of ele-
ments. Two studies that have applied this technique to the transport of lead to remote
areas are Murozumi et al. (1969) and Shirahata et al. (1980). In these studies, the influence
of natural or crustal lead was determined by mass balance, and the relative influence of
023PB6/A
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PRELIMINARY DRAFT
anthropogenic lead was determined. In the Shirahata et al. (1980) study, the influence of
anthropogenic lead was confirmed quantitatively by analysis of isotopic compositions in the
manner of Chow et al. (1975).
Harrison and Williams (1982) determined air concentrations, particle size distributions,
and total deposition flux at one urban and two rural sites in England. The urban site, which
had no apparent industrial, commercial or municipal emission sources, had an air lead
concentration of 3.8 pg/m3, whereas the two rural sites were about 0.15 pg/ms. The average
particle size became smaller toward the rural sites, as the mass median equivalent diameter
(MMED) shifted downward from 0.5 to 0.1 pm. The total deposition flux will be discussed
in Section 6.4.2.
Knowledge of lead concentrations in the oceans and glaciers provides some insight into
the degrees of atmospheric mixing and long range transport. Tatsumoto and Patterson (1963),
Chow and Patterson (1966), and Schaule and Patterson (1980) measured dissolved lead
concentrations in sea water off the coast of California, in the Central North Atlantic (near
Bermuda), and in the Mediterranean, respectively. The profile obtained by Schaule and
Patterson (1980) is shown in Figure 6-4. Surface concentrations in the Pacific (14 ng/kg)
were found to be higher than those of the Mediterranean or the Atlantic, decreasing abruptly
with depth to a relatively constant level of 1 to 2 ng/kg. The vertical gradient was found to
be much less in the Atlantic. Tatsumoto and Patterson (1963) had earlier estimated an average
surface lead concentration of 200 ng/kg in the northern hemispheric oceans. Chow and
Patterson (1966) revised this estimate downward to 70 ng/kg. Below the mixing layer, there
appears to be no difference between lead concentrations in the Atlantic and Pacific. These
investigators calculated that industrial lead currently is being added to the oceans at about
10 times the rate of introduction by natural weathering, with significant amounts being
removed from the atmosphere by wet and dry deposition directly into the ocean. Their data
suggest considerable contamination of surface waters near shore, diminishing toward the open
ocean (Chow and Patterson, 1966).
Duce et al. (1975), Taylor (1964), and Maenhaut et al. (1979) have investigated trace
metal concentrations (including lead) in the atmosphere in remote northern and southern
hemispheric sites. The natural sources for such atmospheric trace metals include the oceans
and the weathering of the Earth's crust, while the anthropogenic source is particulate air
pollution. Enrichment factors for concentrations relative to standard values for the oceans
and the crust were calculated (Table 6-2); the mean crustal enrichment factors for the
North Atlantic and the South Pole are. shown in Figures 6-5 and 6-6. The significance
of the comparison in Figure 6-6 is that 90 percent of the particulate pollutants in the global
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PRELIMINARY DRAFT
1000
• DISSOLVED Pb
~ PARTICULATE Pb
2000 a-
3000
4000 a- >
5000 *4
__l
0 2 4 8 8 10 12 14 18 0
CONCENTRATION, ng Pb/kg
Rgure 6-4. Profile of lead concentrations in the
central northeast Pacific. Values below 1000 m are
an order of magnitude lower than reported by
Tatsumoto and Patterson (1963) and Chow and
Patterson (1966).
Source; Schaule and Patterson (1980).
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023PB6/A
PRELIMINARY DRAFT
60' 40°
ICELAND
GREENLAND •
NORTH ATLANTIC
• AZORES
• V
Figure 6-6. Midpoint collection location for at-
moapharlc eamplee collected from R.V. Trident
north of 30 N, 1970>1972.
Source: Duce et al. (1976b Zoller et el. (1974).
10a
10 '
¦ NORTH ATLANTIC WESTERLIES
-SOUTH POLE
ELEMENT
Figure 6-6. The EFcru.t values for atmospheric
trace metals collected in the North Atlentic
westerlies end at the South Pole. The horizontal
bars represent the geometric mean enrichment fac-
tors, and the vertical bars represent the geometric
standard deviation of the mean enrichment fectors.
The EFcrust for lead at the South Pole is based on
the lowest lead concentration (0.2 mg/scm).
Source: Duce et al. (1975); Zoller et al. (1974).
6-W 7/01/83
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PRELIMINARY DRAFT
troposphere are injected in the northern hemisphere (Robinson and Robbins, 1971). Since the
residence times for particles in the troposphere (Poet et al., 1972) are much less than the
interhemispheric mixing time, it is unlikely that significant amounts of particulate
pollutants can migrate from the northern to the southern hemisphere via the troposphere;
however, this does not rule out stratospheric transfer.
TABLE 6-2. ENRICHMENT OF ATMOSPHERIC AEROSOLS OVER CRUSTAL ABUNDANCE
Using the crustal abundances of Taylor (1964), the enrichment of atmospheric aerosols, rela-
tive to aluminum, has been calculated by Duce et al. (1975). An enrichment factor signifi-
cantly above one implies a source other than crustal rock for the element in question.
Element
Concentration
range, ng/m3
samtsaBsms^Brsssr" mt • r r < | t p--
Enrichment
factor
Al
8-370
1.0
Si
0:0008-0.Oil
0.8
Fe
3.4-220
1.4
Co
0.006-0.09
2.4
Mn
0.05-5.4
2.6
Cr
0.07-1.1
11
V
0.06-14
17
Zn
0.3-27
110
Cu
0.12-10
120
Cd
0.003-0.62
730 .
Pb
0.10-64
2,200
Sb
0.05-0.64
2,300
Se
0.09-0.40
10,000
aBased on the geometric mean of the concentration.
Murozumi et al. (1969) have shown that long range transport of lead particles emitted
from automobiles has significantly polluted the polar glaciers. They collected samples of
snow and ice from Greenland and the Antarctic. As shown in figure 6-7, they found that the
concentration of lead varied inversely with the geological age of the sample. The authors
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PRELIMINARY DRAFT
0.20
0.18
0.16
while the mean concentration in the
Polish glacier reached 148 yg/kg. Jaworowski et al. (1975) attributed the large increase of
lead concentrations in the Polish glacier to local sources.
023PB6/A
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PRELIMINARY DRAFT
Evidence from remote areas of the world suggests that lead and other fine particle
components are transported substantial distances, up to thousands of kilometers, by general
weather systems. The degree of surface contamination of remote areas with lead depends both
on weather influences and on the degree of air contamination. However, even in remote areas,
man's primitive activities can play an important role in atmospheric lead levels. Davidson et
al. (1982) have shown that there are significant levels of fine particle lead, up to 0.5
jjg/m3, in remote villages in Nepal. The apparent source is combustion of dried yak dung,
which contains small amounts of naturally occurring lead derived from plant life in those
remote valleys.
6.3 TRANSFORMATION OF LEAD IN AIR
6.3.1 Particle Size Distribution
Whitby et al. (1975) placed atmospheric particles into three different size regimes: the
nuclei mode (<0.1 pm), the accumulation mode (0.1 to 2 pm) and the large particle mode (>2
jim). At the source, lead particles are generally in the nuclei and large particle modes.
Large particles are removed by deposition close to the source and particles in the nuclei mode
diffuse to surfaces or agglomerate while airborne to form larger particles of the accumulation
mode. Thus it is in the accumulation mode that particles are dispersed great distances.
In Figure 6-8, size distributions for lead particles in automobile exhaust are compared
with those found in air samples at a receptor site in Pasadena, California, "not in the
immediate influence of traffic" (Huntzicker et al., 1975). The authors conclude that the
large particle mode found in exhaust (>9 pm) is severely attenuated in ambient air samples.
Therefore, large particle lead must be deposited near roadways. Similar data and conclusions
had been reported earlier by Oaines et al. (1970).
Pierson and Brachaczek (1976) reported particle size distributions that were larger in
ambient air than in a roadway tunnel, where vehicle exhaust must be dominant (see Figure 6-9).
The large particles may haye been deposited in the roadway itself and small particles may have
agglomerated during transport from the roadway to the immediate roadside. Since 40 to 1,000
pm particles are found in gutter debris (Figure 6-10), deposition of large particles appears
confirmed.
Little and Wiffen (1977, 1978) reported a MMED for lead of 0.1 |jm in the roadway but
0.3 pm 1 meter from the road edge in an intercity expressway in England. Further, particle
size distributions reported by Huntzicker et al. (1975) show binodal distributions for on-
roadway samples, with peak mass values at about 0.1 and 10 pm. For off-roadway Pasadena
samples, there is no evidence of bimodality and only a broad maximum in lead mass between 0.1
and 1 pm.
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PRELIMINARY DRAFT
10.0
e
S
I
w
U
1
8.0
6.0
cc
UJ
k
UJ
4.0
Q
ui
O
2.0
cc
<
a.
u
2
<
z
>
~
o
cc
UI
<
1.0
0.8
0.6
0.4
AUTO EXHAUST
Pb
PASADENA Pb
(11/72)
(2/74)
20 40 60 80 90 95 98
MASS IN PARTICLES < D , percent
Figure 6-8. Cumulative mass distribution for lead particles in
auto exhaust and at an urban site in Pasadena, Calif, some
distance from high traffic density roadways.
Source: Huntzicker et al. (1975).
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PRELIMINARY DRAFT
AMBIENT AER080L Pb
0.6
VEHICLE AEROSOL Pb
0.4
0.2 -
0.1
1
10
80 90 96 98 99
80
% OF MASS IN PARTICLES SMALLER THAN STATED p*d
Figure 6-9. Particulate lead size distribution measured at the
Allegheny Mountain Tunnel, Pennsylvania Turnpike, 1976.
Source: Pierson and Brachaczek (1976).
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1000
500
o
a
100
80
10
0----0 S8R
£>-• — -O 2n
•- « GROSS
U I I till
I I I
MM
0.1 1 2 B 10 60 90 96 98 98 98J
PERCENT OF MASS IN PARTICLES SMALLER THAN STATED SIZE
Figure 6-10. Particle size distributions of substances in gutter
debris. Rotunda Drive, Dearborn, Michigan.
Source: Pierson and Brachaczek (1976).
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In cities or in rural areas, there is a remarkable consistency in lead particle size
range. For example, Robinson and Ludwig (1964) report cascade impactor MMED values for lead
ranging from 0.23 to 0.3 h* in six U.S. cities and three rural areas as shown in Table 6-3.
Stevens et al. (1978) have reported dichotoatous sanpler data for six U.S. cities, as shown in
Table 6-4, and Stevens et al. (1980, 1982) have reported similar results for remote locations.
Virtually every other study reported in the literature for Europe, South America, and Asia has
cone to the conclusion that ambient urban and rural air contains predominantly fine particles
(Cholak et al., 1968; De Jonghe and Adams, 1980; Durando and Aragon, 1982; Lee et al., 1968;
Htun and Ramachandran, 1977).
TABLE 6-3. COMPARISON OF SIZE DISTRIBUTIONS OF LEAD-CONTAINING
PARTICLES IN MAJOR SAMPLING AREAS
Distribution by particle size, um
25Xa
MMED
75%*
No. of
Sample area samples
Avg.
Range
Avg.
Range
Avg.
Range
Chicago
12
0.19(7)b
0.10-0.29
0.30
0.16-0.64
0.40(10)
0.28-0.63
Cincinnati
7
0.15(3)
0.09-0.24
0.23
0.16-0.28
0.44
0.30-0.68
Philadelphia
7
0.14(3)
0.09-0.25
0.24
0.19-0.31
0.41
0.28-0.56
Los Angeles
8
0.16(7)
0.10-0.22
0.26
0.19-0.29
0.49(7)
0.39-0.60
Pasadena
7
0.18
0.05-0.25
0.24
0.08-0.32
0.48(6)
0.13-0.67
San Francisco
3
0.11
0.06-0.13
0.25
0.15-0.31
0.45(2)
0.44-0.46
Vernon (rural)
5
0.17(4)
0.12-0.22
0.24
0.18-0.32
0.40
0.28-0.47
Cherokee (rural)
1
0.25
0.31
0.71
Mojave (rural)
1
-
0.27
0.34
^ refers to the percentile of the mass distribution. Thus in the column labeled 2SK are the
particle sizes at which 25% of the particle mass is in smaller sizes. Similarly, the 75%
.column contains values of particle sizes at which 75% of the mass is in smaller sizes.
Numbers in parentheses Indicate number of samples available for a specific value when dif-
ferent from total number of samples.
Source: Robinson and Ludwig (1964).
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TABLE 6-4. DISTRIBUTION OF LEAD IN TWO SIZE FRACTIONS AT
SEVERAL SITES IN THE UNITED STATES
Cpg/m3)
Location
Date
Fine
Coarse
F/C ratio
New York, NY
2/1977
1.1
0.18
6.0
Philadelphia, PA
2-3/1977
0.95
0.17
5.6
Charlestown, W. WA
4-8/1976
0.62
0.13
4.6
St. Louis, M0
12/1975
0.83
0.24
3.4
Portland, OR
12/1977
0.87
0.17
5.0
Glendora, CA
3/1977
0.61
0.09
6.7
Average
5.2
Source: Stevens et al. (1978).
It appears that lead particle size distributions are stabilized close to roadways and
remain constant with transport into remote environments (Gillette and Winchester, 1972),
6.3.2 Organic (Vapor Phase) Lead in Air
¦mm >i i ip—tmmmm¦
Although lead additives used in gasoline are less volatile than gasoline itself (see
Section 3.4), snail amounts may escape to the atmosphere by evaporation from fuel systems or
storage facilities. Tetraethyllead (TEL) and tetramethyllead (TML) photochemically decompose
when they reach the atmosphere (Huntzicker et al., 1975; National Air Pollution Control
Administration, 1965). The lifetime of TML is longer than that of TEL. Laveskog (1971) found
that transient peak concentrations of organolead up to 5,000 pg/ms in exhaust gas nay be
reached in a cold-started, fully choked, and poorly tuned vehicle. If a vehicle with such
emissions were to pass a sampling station on a street where the lead level might typically be
0.02 to 0.04 yg/ms, a peak of about 0.5 Mg/m3 could be measured as the car passed by. The
data reported by Laveskog were obtained with a procedure that collected very small (100 ml),
short-time (10 m1n) air samples. Harrison et al. (1975) found levels as high as 0.59 jjg/m3
(9.7 percent of total lead) at a busy gasoline service station in England. Grandjean and
Nielsen (1977), using GC-MS techniques, found elevated levels (0.1 hq/h3) of WL in city
streets in Denmark and Norway. These authors attributed these results to the volatility of
TML compared with TEL.
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A number of studies have used gas absorbers behind filters to trap vapor-phase lead
compounds. Because it is not clear thpt.all the lead captured in the backup traps is, in
fact, in the vapor phase in the atmosphere, "organic" or "vapor phase" lead is an operational
definition in these studies. Purdue et al. (1973) measured both particulate and organic lead
in atmospheric samples. They found that the vapor phase lead was about 5 percent of the total
lead in most samples. The results are consistent with the studies of Huntzicker et al. (1975)
who reported an organic component of 6 percent of the total airborne lead in Pasadena for a
3-day period in June, 1974, and of Skogerboe (1975), who measured fractions in the range of 4
to 12 percent at a site in Fort Collins, Colorado. It is noteworthy, however, that in an
underground garage, total lead concentrations were approximately five times those in ambient
urban atmospheres, and the organic lead increased to approximately 17 percent.
Harrison et al. (1979) report typical organolead percentages in ambient urban air of 1 to
6 percent. Sohbock et al. (1980) reported higher fractions, up to 20 percent, but the data
and interpretations have been questioned by Harrison and Laxen (1980). Rohbock et al. (1980)
and De Jonghe and Adams (1980) report one to two orders of magnitude decrease in organolead
concentrations from the central urban areas to residential areas.
5.3.3 Chemical Transformations of Inorganic Lead in Air
Lead is emitted into the air from automobiles as lead halides and as double salts with
ammonium halides (e.g., PbBrCl ~ 2NH4C1). From mines and smelters, PbS04, Pb0*PbS04, and PbS
appear to be the dominant species. In the atmosphere, lead is present mainly as the sulfate
with minor amounts of halides. It is not completely clear just how the chemical composition
changes in transport.
Biggins and Harrison (1978, 1979) have studied the chemical composition of lead particles
in exhaust and in city air in England by X-ray diffractonetry. These authors reported that
the dominant exhaust forms were PbBrCl, PbBrCl*2NH4C1, and a-2PbBrCl*NH4C1, in agreement with
the earlier studies of Hirschler and Gilbert (1964) and Ter Haar and Bayard (1971).
At sampling sites in Lancaster, England, Biggins and Harrison (1978, 1979) found
PbS04-(NH4)2S04, and PbS04*(NH4)2BrCl together with minor amounts of the lead halides and
double salts found in auto exhaust. These authors suggested that emitted lead halides react
with acidic gases or aerosol components (S02 or H2S04) on filters to form substantial levels
of sulfate salts. It is not clear whether reactions with S04 occurs in the atmosphere or on
the sample filter.
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The ratio of Br to Pb is often cited as an indication of automotive emissions. From the
aiixtures commonly used in gasoline additives, ^s^^r/Pb ratio should be about 0.386 if
there has been no fractionation of either element (Harrison and Sturges, 1983). However,
several authors have reported loss of halide, preferentially bromine, from lead salts in
atmospheric transport (Dzubay and Stevens, 1973; Pierrard, 1969; Ter Haar and Bayard, 1971).
Both photochemical decomposition (Lee et a1., 1971; Ter Haar and Bayard, 1971) and acidic gas
displacement (Robbins and Snitz, 1972) have been postulated as mechanisms. Chang et al.
(1977) have reported only very slow decomposition of lead bromochloride in natural sunlight;
currently the add displacement of halide seems to be the most likely mechanism. O'Connor
et al. (1977) have reported no loss in bromine in comparison of roadside and suburban-rural
aerosol samples from western Australia; low levels of S02 and sulfate aerosol could account
for that result. Harrison and Sturges (1983) warn of several other factors that can alter the
Br/Pb ratio. Bromine may pass through the filter as hydrogen bromide gas, lead may be
retained in the exhaust system, or bromine may be added to the atmosphere from other sources,
such as marine aerosols. They concluded that Br/Pb ratios are only crude estimates of
automobile emissions, and that this ratio would decrease with distance from the highway from
0.39 to 0.35 less proximate sites and 0.25 1n suburban residential areas.
Habibi et al. (1970) studied the composition of auto exhaust particles as a function of
particle size. Their main conclusions follow:
1. Chemical composition of emitted exhaust particles is related to
particle size.
a. Very large particles greater than 200 pm have a
composition similar to lead-containing material deposited
In the exhaust system, confirming that they have been
emitted from the exhaust system. These particles contain
approximately 60 to 65 percent lead salts, 30 to 35
percent ferric oxide (Fe203), and 2 to 3 percent soot and
carbonaceous material. The major lead salt is lead
bromochloride (PbBrCl), with (15 to 17 percent) lead oxide
(PbO) occurring as the 2Pb0*PbBrCl double salt. Lead
sulfate and lead phosphate account for 5 to 6 percent of
these deposits. (These compositions resulted from the
combustion of low-sulfur and low-phosphorus fuel.)
b. PbBrCl is the major lead salt in particles of 2 to 10 h**
equivalent diameter, with 2PbBrCl*NH4C1 present as a minor
constituent.
c. Submicrometer-sized lead salts are primarily 2PbBrC1>NH4C1.
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2. Lead-halogen molar, ratios in particles of less than 10 M"> MMED
indicate that much more halogen is associated with these solids
than the amount expected from the presence of 2PbBrCl-NH4C1, as
identified by X-ray diffraction. This is particularly true for
particles in the 0.5 to 2 size range.
3. There is considerably more soot and carbonaceous material
associated with fine-mode particles than with coarse mode
particles re-entrained after having been deposited after
emission from- the exhaust system. This carbonaceous material
accounts for 15 to 20 percent of the fine particles.
4. Particulate matter emitted under typical driving conditions is
rich in carbonaceous material. There is substantially less
such material emitted under continuous hot operation.
5. Only small quantities of 2PbBrCl-NH4C1 were found in samples
collected at the tailpipe from the hot exhaust gas. Its
formation therefore takes place primarily during cooling and
mixing of exhaust with ambient air.
Foster and Lott (1980) used X-ray diffractometry to study the composition of lead
compounds associated with ore handling, sintering, and blast furnace operations around a lead
smelter in Missouri. Lead sulfide was the main constituent of those samples associated with
ore handling and fugitive dust from open mounds of ore concentrate. The major constituents
from sintering and blast furnace operations appeared to be PbS04 and Pb0*PbS04, respectively.
6.4 REMOVAL OF LEAD FROM THE ATMOSPHERE
Before atmospheric lead can have any effect on organisms or ecosystems, it must be
transferred from the air to a surface. For natural ground surfaces and vegetation, this
process may be either dry or wet deposition.
6.4.1 Dry Deposition
6.4.1.1 Mechanisms of Dry Deposition. Transfer by dry deposition requires that the particle
move from the main airstream through the boundary layer to a surface. The boundary layer is
defined as the region of minimal air flow immediately adjacent to that surface. The thickness
of the boundary layer depends mostly on the windspeed and roughness of the surface.
Airborne particles do not follow a smooth, straight path in the airstream. On the
contrary, the path of a particle may be affected by micro-turbulent air currents, gravitation,
or its own inertia. There are several mechanisms which alter the particle path sufficient to
cause transfer to a surface. These mechanisms are a function of particle size, windspeed, and
surface characteristies.
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Particles larger than a few micrometers in diameter are influenced primarily by
sedimentation, where the particle accelerates downward until aerodynamic drag is exactly
balanced by gravitational force. The particle continues at this velocity until it reaches a
surface. Sedimentation is not influenced by windspeed or surface characteristics. Particles
moving in an airstream may be removed by impaction whenever they are unable to follow the
airstream around roughness elements of the surface, such as leaves, branches, or tree trunks.
In this case, the particle moves parallel to the airstream and strikes a surface perpendicular
to the airstream. A related mechanism, turbulent inertia! deposition, occurs when a particle
encounters turbulence within the airstream causing the particle to move perpendicular to the
airstream. It may then strike a surface parallel to the airstream. In two mechanisms, wind
eddy diffusion and interception, the particle remains in the airstream until it is transferred
to a surface. With wind eddy diffusion, the particle 1s transported downward by turbulent
eddies. Interception occurs when the particle in the airstream passes within one particle
radius of a surface. This mechanism Is more a function of particle size than windspeed. The
final mechanism, Brownian diffusion, is important for very small particles at very low
w1ndspeeds. Brownian diffusion is motion, caused by random collision with molecules, in the
direction of a decreasing concentration gradient.
Transfer from the main airstream to the boundary layer is usually by sedimentation or
wind eddy diffusion. From the boundary layer to the surface, transfer may be by any of the
six mechanisms, although those which are independent of windspeed (sedimentation,
interception, Brownian diffusion) are more likely.
6.4.1.2 Dry deposition models. A particle influenced only by sedimentation may be considered
to be moving downward at a specific velocity usually expressed in an/sec. Similarly,
particles transported to a surface by any mechanism are said to have an effective deposition
velocity (Vd), which is measured not by rate of particle movement but by accumulation on a
surface as a function of air concentration. This relationship is expressed in the equation:
vd = J/C
where J is the flux or accumulation expressed in ng/cmz*s and C is the air concentration in
ng/cm3. The units of Vd become cm/sec.
Several recent models of dry deposition have evolved from the theoretical discussion of
Fuchs (1964) and the wind tunnel experiments of Chamberlain (1966). From those early works,
1t was obvious that the transfer of particles from the atmosphere to the Earth's surface
involved more than rain or snow. The models of SI inn (1982) and Davidson et al. (1982)
are particularly useful for lead deposition and were strongly influenced by the theoretical
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PRELIMINARY DRAFT
discussions of fluid dynamics by Friedlander (1977). Slinn's node! considers a multitude of
vegetation parameters to find several approximate solutions for particles in the size range of
0.1 to 1.0 pm. In the absence of appropriate field studies, Slinn (1982) estimates deposition
velocities of 0.01 to 0.1 cm/sec.
The model of Oavidson et al. (1982) is based on detailed vegetation measurements and wind
data to predict a Vd of 0.05 to 1.0 cm/sec. Deposition velocities are specific for each
vegetation type. This approach has the advantage of using vegetation parameters of the type
made for vegetation analysis in ecological studies (density, leaf area index (LAI), height,
diameter) and thus may be applicable to a broad range of vegetation types for which data are
already available in the ecological literature.
Both models show a decrease in deposition velocity with decreasing particle size down to
about 0.1 to 0.2 pm, followed by an increase in with decreasing diameter from 0.1 to 0.001
cm/sec. On a log plot of diameter vs. V^, this curve is v-shaped, and the plots of several
vegetation types show large changes (10X) in minimum Vd, although the minima commonly occur at
about the same particle diameter (Figure 6-11).
In summary, it is not correct to assume that air concentration and particle size alone
determine the flux of lead from the atmosphere to terrestrial surfaces. The type of vegetation
canopy and the influence of the canopy on windspeed are important predictors of dry
deposition. Both of these models predict deposition velocities more than one order of
magnitude lower than reported in several earlier studies (e.g., Sehmel and Hodgson, 1976).
6.4.1.3 Calculation of Dry Deposition. The data required for calculating the flux of lead
from the atmosphere by dry deposition are leaf area index, windspeed, deposition velocity, and
air concentration by particle size. The LAI should be total surface rather than upfacing
surface, as used in photosynthetic productivity measurements. Leaf area indices should also
be expressed for the entire community rather than by individual plant, in order to incorporate
variations in density. Some models use a more generalized surface roughness parameter, 1n
which case the deposition velocity may also be different.
The value selected for depends on the type of vegetation, usually described as either
short (grasses or shrubs) or tall (forests). For particles with an MMED of about 0.5, Hicks
(1980) gives values for tall vegetation deposition velocity from 0.1 to 0.4 cm/sec. Lannefors
and Hansson (1983) estimated values of 0.2 to 0.5 cm/sec in the particle size range of 0.06 to
2.0 pm in a coniferous forest. For lead, with an HMED of 0.55 pm, they measured a deposition
velocity of 0.41.
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p-4
UPPER LIMIT:
NO RESISTANCE BELOW AND
ATMOSPHERIC DIFFUSION FROM
1 on TO 1 m
p-1
LOWER LIMIT:
ONLY BR OWN IAN BELOW AND
ATMOSPHERIC DIFFUSION ABOVE
\ ^ INDICATED HE IOHT
STABLE ATMOSPHERE
WITH ROUGHNESS
\ HEIGHT, cm ,
,0.01 em
10
s
1
0.1
,1 em
p- PARTICLE DENSITY
zQ • ROUGHNESS HEIGHT
M. • FRICTION VELOCITY
K-V.
PARTICLE DIAMETER, m
Figure 6-11. Predicted deposition velocities at 1 m for 30 cm s"'
and particle densities of 1,4, and 11.6 g cm-1.
Source; Sehmel (1980).
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6.4.1.4 Field Measurements of Dry Deposition on Surrogate and Natural Surfaces. Several in-
vestigators have used surrogate surface devices similar to those described in Section 4.2.2.4,
These data are summarized in Table 6-5. The few studies available on deposition to vegetation
surfaces show deposition rates comparable to those of surrogate surfaces and deposition velo-
cities in the range predicted by the models discussed above. In Section 6.4.3, these data are
used to show that global emissions are in approximate balance with global deposition. It is
reasonable that future refinements of field measurements and model calculations will permit
more accurate estimates of dry deposition in specific regions or under specific environmental
conditions.
TABLE 6-5. SUMMARY OF SURROGATE AND VEGETATION SURFACE DEPOSITION OF LEAO
Depositional surface
Flux
ng Pb/cm2*day
Air cone
ng/m3
Deposition velocity
cm/sec
Reference
Tree leaves (Paris)
0.38
0.086
1
Tree leaves (Tennessee)
0.29-1.2
___
2
Plastic disk (remote
California)
0.02-0.08
13-31
0.05-0.4
3
Plastic plates
(Tennessee)
0.29-1.5
110
0.05-0.06
4
Tree leaves (Tennessee)
___
110
0.005
4
Snow (Greenland)
0.004
0.1-0.2
0.1
5
Grass (Pennsylvania)
...
590
0.2-1.1
6
Coniferous forest (Sweden) 0.74
21
0.41
7
1. Servant, 1975.
2. lindberg et al., 1982.
3. Elias and Davidson, 1980.
4. Lindberg and Harriss, 1981.
5. Davidson et al., 1981.
6. Davidson et al., 1982.
7. Lannefors et al., 1983.
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6.4.2 Wet Deposition
Wet deposition includes removal by rainout and washout. Rainout occurs when particulate
natter is present in the supersaturated environment of a growing cloud. The snail particles
(0.1 to 0,2 put) act as nuclei for the formation of small droplets, which grow into raindrops
(Junge, 1963). Droplets also collect particles under 0.1 pm by Brownian Motion and by the
water-vapor gradient. The nucleation process nay also occur on particulate latter present
below cloud level, producing droplets large enough to be affected by sedimentation. These
processes are referred to as rainout. Washout, on the other hand, occurs when falling
raindrops collect particles by diffusion and impaction on the way to the ground. Although
data on the lead content of precipitation are rather limited, those that do exist indicate a
high variability.
Results on lead scavenging by washout are conflicting. In a laboratory study employing
simulated rainfall, Edwards (1975) found that less than 1 percent of auto exhaust lead
particles could be removed by washout. However, Ter Haar et al. (1967) found that intense
rainfall removed most of the atmospheric lead. As a result, the lead content of rain water is
smaller for intense rainfall than in steady showers, presumably because the air contains
progressively less lead. It is not clear which of the two phenomena, nucleation or washout,
is responsible.
lazrus et al. (1970) sampled precipitation at 32 U.S. stations and found a correlation
between gasoline used and lead concentrations in rainfall in each area. Similarly, there is
probably a correlation between lead concentration in rainfall and distance from large
stationary point sources. The authors pointed out that at least twice as much lead is found
in precipitation as in water supplies, implying the existence of a process by which lead is
removed from the soil solution after precipitation reaches the ground. Russian studies
(Konovalov et al., 1966) point to the insolubility of lead compounds in surface waters and
suggest removal by natural sedimentation and filtration.
Atkins and Kruger (1968) conducted a field sampling program in Palo Alto, California, to
determine the effectiveness of sedimentation, impaction, rainout, and washout in removing lead
from the atmosphere. Rainfall in the area averages approximately 33 cm/year and occurs
primarily during the late fall and winter months. Airborne concentrations at a freeway site
varied from 0.3 pg/m3 to a maximum of 19 pg/m* in the fall and winter seasons, and were a
maximum of 9.3 pg/m3 in the spring. During periods of light rainfall in the spring, the
maximum concentration observed was 7.4 pg/m3. More than 90 percent of the lead reaching the
surface during the one-year sampling period was collected in dry fallout. Wet deposition
accounted for 5 to 10 percent of the lead removal at the sampling sites.
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Andren et al. (1975) evaluated the contribution of wet and dry deposition of lead in a
study of the Walker Branch Watershed in Oak Ridge, Tennessee, during the period June 1973 to
July 1974. The mean precipitation in the area is approximately 130 cm/yr. Results reported
for the period January through June 1974 are presented in Table 6-6. Wet deposition
contributed approximately 67 percent of the total deposition for the period.
TABLE 6-6. DEPOSITION OF LEAD AT THE WALKER BRANCH WATERSHED, 1974
Lead deposition (g/ha)
Period
Wet
Dry
January
34.1
<16.7
February
6.7
< 3.3
March
21.6
<10.6
April
15.4
< 7.5
May
26.5
<13.0
June
11.1
< 5.4
Total
115.4
56.5
Average
19.2
9.4
aTotal deposition ~172 g/ha. Wet deposition ~67 percent of total.
Source: Andren et al., 1975.
6.4.3 Global Budget of Atmospheric Lead
The geochemical mass balance of lead in the atmosphere may be determined from
quantitative estimates of inputs and outputs. Inputs are from natural and anthropogenic
emissions described in Section 5.2 and 5.3. They amount to 450,000 to 475,000 metric tons
annually (Nriagu, 1979). There are no published estimates of global deposition from the
atmosphere, but the data provided in Sections 6.4.1 and 6.4.2 can provide a reasonable basis
on which to make such an estimate. Table 6-7 shows an average concentration of 0.4 M0 Pb/kg
precipitation. The total mass of rain and snowfall is 5.2 x 107 kg, so the amount of lead
removed by wet deposition is approximately 208,000 t/yr. For dry deposition, a crude estimate
may be derived by dividing the surface of the Earth into three major vegetation types based on
surface roughness or LAI. Oceans, polar regions, and deserts have a very low surface rough-
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TABLE 6-7. ESTIMATED -GLOBAL DEPOSITION OF ATMOSPHERIC LEAD
Deposition from atmosphere
Mass Concentration
10" kg/yr
10"6 g/kg
Deposition
10* kg/yr
Wet
To oceans
To continents
Dry
4.1
1.1
Area
1012 km2
To oceans, ice caps, deserts 405
Grassland, agricultural
areas, and tundra 46
Forests 59
0.4
0.4
Deposition rate
10 3 g/m2»yr
0.2
0.71
1.5
Total dry:
Total wet:
Global:
164
44
Deposition
106 kg/yr
89
33
80
202
208
410
Source: This report.
ness and can be assigned a deposition velocity of 0.01 on/sec, which gives a flux of 0.2
pg/n^-yr assuming 75 ng Pb/m3 air concentration. Grasslands, tundra, and other areas of
low-lying vegetation have a somewhat higher deposition velocity; forests would have the
highest. Values of 0.3 and 0.65 can be assigned to these two vegetation types, based on the
data of Davidson et al. (1982). Vfliittaker (1975) lists the global surface area of each of the
three types as 405, 46, and 59 x 1012 km2, respectively. In the absence of data on the global
distribution of air concentrations of lead, an average of 0.075 pg/m3 is assuned. Multiplying
air concentration by deposition.velocity gives the deposition flux for each vegetation type
shown on Table 6-7. The combined wet and dry deposition is 410,000 metric tons, which
compares favorably with the estimated 450,000 to 475,000 metric tons of enissions.
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distributions represent the most extensive size distribution data base available. However,
the impactors were operated at excessive air flow rates that most likely resulted in particle
bounceoff, biasing the data toward smaller particles (Dzubay et al., 1976). Many of the later
distributions, although obtained by independent investigators with unknown quality control,
were collected using techniques which minimize particle bounceoff and hence may be more reli-
able. It is important to note that a few of the distributions were obtained without backup
filters that capture the smallest particles. These distributions are likely to be inaccurate,
since an appreciable fraction of the airborne lead mass was probably not sampled. The distri-
butions of Figure 7-5 have been used with published lung deposition data to estimate the frac-
tion of inhaled airborne lead deposited in the human respiratory system (see Chapter 10).
7.2.1.3.2 Vertical gradients and siting guidelines. New guidelines for placing ambient air
lead monitors went into effect in July, 1981 (F.R., 1981). "Microscale" sites, placed between
5 and 15 meters from thoroughfares and 2 to 7 meters above the ground, are prescribed, but
until now few monitors have been located that close to heavily traveled roadways. Many of
these microscale sites might be expected to show higher lead concentrations than that measured
at nearby middlescale urban sites, due to vertical gradients in lead concentrations near the
source. One study (PEDCo, 1981) gives limited insight into the relationship between a micro-
scale location and locations further from a roadway. The data in Table 7-6 summarize total
suspended particulates and particulate lead concentrations in samples collected in Cincinnati,
Ohio, on 21 consecutive days in April and May, 1980, adjacent to a 58,500 vehicles-per-day
expressway connector. Simple interpolation indicates that a microscale monitor as close as 5
meters from the roadway and 2 meters abo.ve the ground would record concentrations some 20 per-
cent higher than those at a "middle scale" site 21.4 meters from the roadway. On the other
hand, these data also indicate that although lead concentrations very close to the roadway
(2.8 m setback) are quite dependent on the height of the sampler, the averages at the three
selected heights converge rapidly with increasing distance from the roadway. In fact, the
average lead concentration (1.07 ng/ms) for the one monitor (6.3 a height, 7.1 m setback) that
satisfies the microscale site definition proves not to be significantly different from the
averages for its two companions at 7.1 n, or from the averages for any of the three monitors
at the 21.4 m setback. It also appears that distance from the source, whether vertical or
horizontal, can be the primary determining factor for changes in air lead concentrations. At
7,1 ¦ from the highway, the 1.1 and 6.3 m samplers would be about 7 and 11 meters from the
road surface. The values at these vertical distances are only slightly lower than the
corresponding values for comparable horizontal distances.
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Mass balance calculations of this type serve to accentuate possible errors in the data
which are not otherwise obvious. The data used above are not held to be absolutely firm.
Certainly, more refined estimates of air concentrations and deposition velocities can be nade
in the future. On the other hand, the calculations above show some published calculations to
be unreasonable. In particular, values of 36 Mg/kg rain reported by Lazrus (1970) would
account for more than 50 tines the total global emissions. Likewise, deposition fluxes of
0.95 MSJ/cm^yr reported by Jaworowski et al. (1981) would account for 10 times global
emissions. Chemical budgets are an effective means of establishing reasonable limits to
environmental lead data.
6.5 TRANSFORMATION AND TRANSPORT IN OTHER ENVIRONMENTAL MEDIA
6.5.1 Soil
Soils have both a liquid and solid phase, and trace metals are normally distributed
between these two phases. In the liquid phase, metals may exist as free ions or as soluble
complexes with organic or inorganic ligands. Organic ligands are typically humic substances
such as fulvic or humic acid, and the inorganic ligands may be iron or manganese hydrous
oxides. Since lead rarely occurs as a free ion in the liquid phase (Camerlynck and Kiekens,
1982), its mobility in the soil solution depends on the availability of organic or Inorganic
ligands. The liquid phase of soil often exists as a thin film of moisture in intimate contact
with the solid phase. The availability of metals to plants depends on the equilibrium between
the liquid and solid phase.
In the solid phase, metals may be incorporated into crystalline minerals of parent rock
material, into secondary clay minerals, or precipitated as insoluble organic or inorganic
complexes. They may also be adsorbed onto the surfaces of any of these solid forms. Of these
categories, the most mobile form is in soil moisture, where lead can move freely into plant
roots or soil microorganisms with dissolved nutrients. The least mobile is parent rock
material, where lead may be bound within crystalline structures over geologic periods of time.
Intermediate are the lead complexes and precipitates. Transformation from one form to another
depends on the chemical environment of the soil. For example at pH 6 to 8, insoluble
organic-Pb complexes are favored if sufficient organic matter is available; otherwise hydrous
oxide complexes may form or the lead may precipitate with the carbonate or phosphate ion. In
the pH range of * to 6, the organic-Pb complexes become soluble. Soils outside the pH range
of 4 to 8 are rare. The interconversion between soluble and insoluble organic complexes
affects the equilibrium of lead between the liquid and solid phase of soil.
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Even though the equilibrium may shift toward the insoluble form so strongly that 99.9
percent of the lead may be immobilized, 0.01 percent of the lead in total soil can have a
significant effect on plants and microorganisms if the soils are heavily contaminated with
lead (Chapter 8).
The water soluble and exchangeable forms of metals are generally considered available for
plant uptake (Camerlynck and Kiekens, 1982). These authors demonstrated that in normal soils,
only a small fraction of the total lead is in exchangeable form (about 1 fjg/g) and none exists
as free lead ions. Of the exchangeable lead, 30 percent existed as stable complexes, 70
percent as labile complexes. The organic content of these soils was low (3.2 percent clay,
8.5 percent silt, 88.3 percent sand). In heavily contaminated soils near a Midwestern
industrial site, Miller and McFee (1983) found that 77 percent of the lead was in
exchangeable or organic form, although still none could be found in aqueous solution. Soils
had a total lead content from 64 to 360 Mfl/g and an organic content of 7 to 16 percent.
Atmospheric lead may enter the soil system by wet or dry deposition mechanisms described
earlier. There is evidence that this lead enters as PbS04 or is rapidly converted to PbS04 at
the soil surface (Olson and Skogerboe, 1975). Lead sulfate is relatively soluble and thus
could remain mobile if not transformed. Lead could be immobilized by precipitation as less
soluble compounds [PbC03, Pb(P04)2], by ion exchange with hydrous oxides or clays, or by
chelation with humic and fulvic acids. Santillan-Medrano and Jurinak (1975) discussed the
possibility that the mobility of lead is regulated by the formation of Pb(0H)2, Pb3(P04)2,
Pb5(P04)30H, and PbC0a. This model, however, did not consider the possible influence of
organic matter on lead immobilization. Zimdahl and Skogerboe (1977), on the other hand, found
lead varied linearly with cation exchange capacity (CEC) of soil at a given pH, and linearly
with pH at a given CEC (Figure 6-12). The relationship between CEC and organic carbon is
discussed below.
Some of the possible mechanisms mentioned above can be eliminated by experimental
evidence. If surface adsorption on clays plays a major role in lead Immobilization, then the
capacity to immobilize should vary directly with the surface-to-volume ratio of clay. Two
separate experiments using the nitrogen BET method for determining surface area and size
fractionation techniques to obtain samples with different surface-to-volume ratios, Zimdahl
and Skogerboe (1977) demonstrated that this was not the case. They also showed that precipi-
tation as lead phosphate or lead sulfate is not significant, although carbonate precipitation
can be important in soils that are are carbonaceous in nature or to which lime (CaC0a) has
been added.
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Of the two remaining processes, lead immobilization is more strongly correlated with
organic chelation than with iron and manganese oxide formation (Zimdahl and Skogerboe, 1977).
It is possible, however, that chelation with fulvie and humic acids is catalyzed by the
presence of iron and manganese oxides (Saar and Weber, 1982). This would explain the positive
correlation for both mechanisms observed by Zimdahl and Skogerboe (1977). The study of Miller
and McPee (1983) discussed above seemed to indicate that atmospheric lead added to soil 1s
distributed to organic matter (43 percent) and ferro-manganese hydrous oxides (39 percent),
with 8 percent found in the exchangeable fraction and 10 percent as insoluble precipitates.
If organic chelation is the correct model of lead immobilization in soil, then several
features of this model merit further discussion. First, the total capacity of soil to
immobilize lead can be predicted from the linear relationship developed by Zimdahl and
Skogerboe (1977) (Figure 6-12) based on the equation:
N = 2.8 x 10"e (A) ~ 1.1 x 10'5 (8) - 4.9 x 10"s
where N is the saturation capacity of the soil expressed in moles/g soil, A is the CEC of the
soil in meq/100 g soil, and B is the pH. Because the CEC of soil 1s more difficult to
determine than total organic carbon, it is useful to define the relationship between CEC and
organic content. Pratt (1957) and Klemmedson and Jenny (1966) found a linear correlation
between CEC and organic carbon for soils of similar sand, silt, and clay content. The data of
Zimdahl and Skogerboe (1977) also show this relationship when grouped by soil type. They show
that sandy clay loam with an organic content of 1.5 percent might be expected to have a CEC of
12 meq/100 g. From the equation, the saturation capacity for lead in soil of pH 5.5 would be
45 pmoles/g soil or 9,300 pg/g. The same soil at pH 4.0 would have a total capacity of 5,900
M9/g.
The soil humus model also facilitates the calculation of lead in soil moisture using
values available 1n the literature for conditional stability constants with fulvic acid. The
term conditional is used to specify that the stability constants are specific for the
conditions of the reaction. Conditional stability constants for HA and FA are comparable.
The values reported for log K are linear in the pH range of 3 to 6 (Buffie and Greter, 1979;
Buffie et al., 1976; Greter et al., 1979), so that Interpolations In the critical range of pH
4 to 5.5 are possible (Figure 6-12). Thus, at pH 4.5, the ratio of complexed lead to ionic
lead is expected to be 3.8 x 10s. For soils of 100 pg/g, the ionic lead in soil moisture
solution would be 0.03 pg/g. The significance of this ratio is discussed in Section 8.2.1.
It is also important to consider the stability constant of the Pb-FA complex relative to
other metals. Schnitzer and Hansen (1970) showed that at pH 3, Fes+ is the most stable in the
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pH =- 8
60 76
CEC, nwq/100 g
126
Figure 6-12. Variation of (sad saturation capacity with cation exchange
capacity in soil at selected pH values.
Source: Data from Zimdahl and Skogerboe (19771.
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sequence Fe3+ > A13+ > Cu2+ > Ni2+ > Co2+ > Pb2+ > Ca2+ > Zn2+ > Mn2+ > Mg2+. At pH 5, this
sequence becomes N12+ = Co2* > Pb2+ > Cu2+ > Zn2+ = Mn2+ > Ca2+ > Mg2+. This means that at
normal soil pH levels of 4.5 to 8, lead is bound to FA + HA in preference to many other metals
that are known plant nutrients (Zn, Mn, Ca, and Mg). Furthermore, if lead displaces iron in
this scheme, an important function of FA may be inhibited at near saturation capacity. Fulvic
acid 1s believed to play a role in the weathering of parent rock material by the removal of
iron from the crystalline structure of the minerals, causing the rock to weather more rapidly.
In the absence of this process, the weathering of parent rock material and the subsequent
release of nutrients to soil would proceed more slowly.
6.5.2 Water
6-5.2.1 Inorganic. The chemistry of lead in an aqueous solution is highly complex because
the element can be found in a multiplicity of forms. Hem and Durum (1973) have reviewed the
chemistry of lead in water in detail; the aspects of aqueous lead chemistry that are germane
to this document are discussed in Section 3.3.
Lead in ore deposits does not pass easily to ground or surface water. Any lead dissolved
from primary lead sulfide ore tends to combine with carbonate or sulfate ions to (1) form
insoluble lead carbonate or lead sulfate, or (2) be absorbed by ferric hydroxide (Lovering,
1976). An outstanding characteristic of lead is its tendency to form compounds of low
solubility with the major anions of natural water. Hydroxide, carbonate, sulfide, and more
rarely sulfate may act as solubility controls in precipitating lead from water. The amount of
lead that can remain in solution is a function of the pH of the water and the dissolved salt
content. Equilibrium calculations show that at pH > 5.4, the total solubility of lead in hard
water is about 30 ng/1 and about 500 pg/1 in soft water (Davies and Everhard, 1973). Lead
sulfate is present in soft water and limits the lead concentration in solution. Above pH 5.4,
PbC08 and Pb2(QH)aC0s limit the concentration. The carbonate concentration is in turn
dependent on the partial pressure of C02 as well as the pH. Calculations by Hem and Durum
(1973) show that many river waters in the United States have lead concentrations near the
solubility limits imposed by their pH levels and contents of dissolved COjj. Because of the
influence of temperature on the solubility of C02, observed lead concentrations may vary sig-
nificantly from theoretically calculated ones.
Lazrus et al. (1970) calculated that as much as 140 g/ha-mo of lead may be deposited by
rainfall in some parts of the northeastern United States. Assuming an average annual rainfall
runoff of 50 cm, the average concentration of lead in the runoff would have to be about
330 pg/1 to remove the lead at the rate of 140 g/ha*mo. Concentrations as high as 330 pg/1
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could be stable in water with pH near 6.5 arid an alkalinity of about 25 ng bicarbonate ion/1
of water. Water having these properties is common in runoff areas of New York State and New
England; hence, the potential for high lead concentrations exists there. In other areas, the
average pH and alkalinity are so high that maximum concentrations of lead of about 1 yg/1
could be retained in solutions at equilibrium (Lovering, 1976).
A significant fraction of the lead carried by river water may be in an undissolved state.
This insoluble lead can consist of colloidal particles in suspension or larger undissolved
particles of lead carbonate, -oxide, -hydroxide, or other lead compounds incorporated in other
components of particulate lead from runoff; it may occur either as sorbed ions or surface
coatings on sediment mineral particles or be carried as a part of suspended living or
nonliving organic matter (Lovering, 1976). A laboratory study by Hem (1976) of sorption of
lead by cation exchange indicated that a major part of the lead in stream water nay be
adsorbed on suspended sediment. Figure 6-13 illustrates the distribution of lead outputs
between filtrate and solids in water from both urban and rural streams, as reported by Rolfe
and Jennett (1S75). The majority of lead outpu^ is associated with suspended solids in both
urban and rural streams, with very little dissolved in the filtrate. The ratio of lead in
suspended solids to lead in filtrate varies from 4:1 in rural streams to 27:1 in urban
streams.
Soluble lead is operationally defined as that fraction which is separated from the
insoluble fraction by filtration. However, most filtration techniques do not remove all
colloidal particles. Upon acidification of the filtered sample, which is usually done to
preserve it before analysis, the colloidal material that passed through the filter is
dissolved and is reported as dissolved lead. Because the lead in rainfall can be mainly
particulate, it 1s necessary to obtain more information on the amounts of lead transported in
insoluble form (Lovering, 1976) before a valid estimate can be obtained of the effectiveness
of runoff in transporting lead away from areas where it has been deposited by atmospheric
fallout and rain.
6.5.2.2 Organic. The bulk of organic compounds in surface waters originates from natural
sources. (Neubecker and Allen, 1983). The humic and fulvic acids that are primary complexing
agents in soils are also found 1n surface waters at concentrations from 1 to 5 mg/1,
occasionally exceeding 10 mg/1. (Steelnik, 1977), and have approximately the same chemical
characteristics (Reuter and Perdue, 1977). The most common anthropogenic organic compounds
are NTA and EDTA (Neubecker and Allen, 1983). There are many other organic compounds such as
oils, plasticizers, and polymers discharged from manufacturing processes that nay complex with
lead.
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suspended solids
FILTRATE
100
75
SO
25
WW
li 1111 It r I
URBAN
RURAL
Figure 6-13. Lead distribution between filtrate and suspended
solids in stream water from urban and rural comportments.
Source: Hem (1976); Rolfe and Jennett (1975).
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The presence of fulvic acid in water has been shown to increase the rate of solution of
lead sulfide 10 to 60 times over that of a water solution at the same pH that did not contain
fulvic acid (Bondarenko, 1968; Lovering, 1976). At pH values near 7, soluble lead-fulvic acid
complexes are present in solution. At initial pH values between 7.4 and about 9, the
lead-fulvic acid complexes are partially decomposed, and lead hydroxide and carbonate are
precipitated. At initial pH values of about 10, the lead-fulvic acid complexes again
increase. This Increase is attributed to dissociation of phenolic groups at high pH values,
which increases the complexing capacity of the fulvic acid. But it also may be due to the
formation of soluble lead-hydroxyl complexes.
The transformation of Inorganic lead, especially in sediment, to tetramethyllead (TML)
has been observed and biomethylation has been postulated (Schmidt and Huber, 1976; Wong et
al., 1975). However, Reisinger et al. (1981) have reported extensive studies of the
¦ethylation of lead in the presence of numerous bacterial species known to alkylate mercury
and other heavy metals. In these experiments no biological methylation of lead was found
under any condition. Chemical alkylation from methylcobalamine was found to occur in the
presence of sulfide or of aluminum ion; chemical methylation was independent of the presence
of bacteria.
Jarvie et al. (1977, 1981) have recently shown that tetraalkyllead (TEL) compounds are
unstable in water. Small amounts of Ca2+ and Fe2+ ions and sunlight have been shown to cause
decomposition of TEL over time periods of 5 to 50 days. The only product detected was
triethyllead, which appears to be considerably more stable than the TEL. Tetramethyllead is
decomposed much more ^rapidly than TEL in water, to form the trimethyl lead ion. Initial
concentrations of 10 molar were reduced by one order of magnitude either in the dark or
light in one day, and were virtually undetectable after 21 days. Apparently, chemical
¦ethylation of lead to the trialkyHead cation does occur in some water systems, but evolution
of TML appears insignificant.
Lead occurs in riverine and estuarial waters and alluvial deposits. Laxen and Harrison
(1977) and Harrison and Laxen (1981) found 1arge CBrtcaffltvations of lead (~1 mg/1) in rainwater
runoff from a roadway; but only 5 to 10 percent of this is soluble in water. Concentrations
of lead in ground water appear to decrease logarithmically with distance from a roadway.
Rainwater runoff has been found to be an important transport mechanism in the removal of lead
from a roadway surface in a number of studies (Bryan, 1974; Harrison and Laxon, 1981; Hedley
and Lockley, 1975; Laxen and Harrison, 1977).
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Apparently, only a light rainfall, 2 to 3 m, 1s sufficient to remove 90 percent of the lead
from the road surface to surrounding soil and to waterways (Laxen and Harrison, 1977).
The Applied Geochemistry Research Group (1978) has reported elevated lead concentrations
<40 Hfl/9 and above) in about 30 percent of stream bed sediment samples from England and Wales
in a study of 50,000 such samples. Abdullah and Royle (1973) have reported lead levels in
coastal areas of the Irish sea of 400 Mg/fl and higher.
Evidence for the sedimentation of lead in freshwater streams may be found in several
reports. Laxen and Harrison (1983) found that lead in the effluent of a lead-acid battery
plant near Manchester, England, changed drastically in particle size. In the plant effluent,
53 percent of the lead was on particles smaller than 0.015 (j» and 43 percent on particles
greater than 1 Just downstream of the plant, 91 percent of the lead was on particles
greater ihan 1 pm and only 1 percent on particles smaller than 0.015 pm. Under these
conditions, lead formed or attached to large particles at a rate exceeding that of Cd, Cu, Fe
or Mn.
The lead concentrations in off-shore sediments often show a marked increase corresponding
to anthropogenic activity in the region (Section 5.1). Rippey et al. (1982) found such
increases recorded 1n the sediments of Lough Neagh, Northern Ireland, beginning during ttie
1600's and increasing during the late 1800's. Corresponding Increases were also observed for
Cr, Cu, Zn, Hg, P, and N1. For lead, the authors found an average anthropogenic flux of 72
mg/m2*yr, of which 27 mg/m2»yr could be attributed to direct atmospheric deposition. Prior to
1650, the total flux was 12 mg/m2'yr, so there has been a 6-fold Increase since that time.
Ng and Patterson (1982) found prehistoric fluxes of 1 to 7 mg Pb/m^yr to three offshore
basins in southern California, which have now increased 3 to 9-fold to 11 to 21 mg/m2-yr.
Much of this lead is deposited directly from sewage outfalls, although at least 25 percent
probably comes from the atmosphere.
6.5.3 Vegetation Surfaces
The deposition of lead on the leaf -surfaces of plants where the particles are often
retained for a long time must also be considered (Oedolph et al., 1970; Gange and Joshl, 1971;
Schuck and Locke, 1970). Several studies have shown that plants near roadways exhibit
considerably higher levels of lead than those further aw«y. In most instances, the higher
concentrations were due to lead particle deposition on plant surfaces (Schuck and Locke,
1970). Studies have shown that particles deposited on plant surfaces are difficult to remove
by typical kitchen washing techniques. (Arvik and Zimdahl, 1974; Gange and Joshl, 1971;
Lagerwerff et al., 1973). Leaves with pubescent surfaces seem able to attract and retain
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particles via an electrostatic mechanism.. Other types of leaves are covered with a cuticular
wax sufficiently sticky to retain particles. Thus, rainfall does not generally remove the
deposited particles (Arvlk and Zimdahl, 1974). Animals or humans consuming the leafy portions
of such plants can certainly be exposed to higher than normal levels of lead. Fortunately, a
major fraction of lead emitted by automobiles tends to be deposited inside a highway
right-of-way, so at least part of this problem is alleviated.
The particle deposition on leaves has led some investigators to stipulate that lead may
enter plants through the leaves. This would typically require, however, that the lead
particles be dissolved by constituents of the leaf surface and/or converted to the ionic form
via contact with water. The former possibility is not considered likely since cuticular waxes
are relatively chemically inert. Arvik and Zimdahl (1974) have shown that entry of ionic lead
through plant leaves is of minimal importance. Using the leaf cuticles of several types of
plants essentially as dialysing membranes, they found that even high concentrations of lead
ions would not pass through the cuticles into distilled water on the opposite side.
The uptake of soluble lead by aquatic plants can be an important mechanism for depleting
lead concentrations in downstream waterways. Gale and Wixson (1979) have studied the
influence of algae, cattails, and other aquatic plants on lead and zinc levels in wastewater
in the New Lead Belt of Missouri. These authors report that mineral particles become trapped
by roots, stems, and filaments of aquatic plants. Numerous anionic sites on and within cell
walls participate in cation exchange, replacing metals such as lead with Na+, K+, and H+ ions.
Mineralization of lead in these Missouri waters may also be promoted by water alkalinity.
However, construction of stream meanders and settling ponds have greatly reduced downstream
water concentrations of lead, mainly because of absorption 1n aquatic plants (Gale and Wixson,
1979).
6.6 SUMMARY
From the source of emission to the site of deposition, lead particles are dispersed by
the flow of the airstream, transformed by physical and chemical processes, and removed from
the atmosphere by wet or dry deposition. Under the simplest of conditions (smooth, flat
terrain), the dispersion of lead particles has been modeled and can be predicted (Benarle,
1980). Dispersion modeling in complex terrains is still under development and these models
have not been evaluated (Kotake and Sano, 1981).
Air lead concentrations decrease logarithmically away from roadways (Edwards, 1975) and
smelters (Roberts et al., 1974). Within urban regions, air concentrations decrease from the
central business district to the outlying residential areas by a factor of 2 to 3. In moving
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from urban to rural areas, air concentrations decrease from 1 to 2 pg/m3 down to 0.1 to 0.5
pg/m3 (Chapter 7). This decrease is caused by dilution with clean air and removal by
deposition. During dispersion to remote areas, concentrations decrease to 0.01 pg/m3 in the
United States (Elias and Davidson, 1980), to 0.001 pg/m3 in the Atlantic Ocean (Duce et al.,
1975), and to 0.000076 Mg/*>3 1" Antarctica (Maenhaut et al., 1979).
Physical transformations of lead particles cause a shift in the particle size
distribution. The bimodal distribution of large and small particles normally found on the
roadway changes to a single mode of intermediate sized particles with time and distance
(Huntzicker et al., 1975). This is probably because large particles deposit near roadways and
small particles agglomerate to medium sized particles with an MMED of about 0.2 to 0.3 pm.
Particles transform chemically from lead halides to lead sulfates and oxides. Organolead
compounds usually constitute 1 to 6 percent of the total airborne lead in ambient urban air
(Harrison et al., 1979).
Wet deposition accounts for about half of the removal of lead particles from the
atmosphere. The mechanisms may be rainout, where the lead may be from another region, or
washout, where the source may be local. The other half of the atmospheric lead is removed by
dry deposition. Mechanisms may be gravitational for large particles or a combination of
gravitational and wind-related mechanisms for small particles (Elias and Davidson, 1980).
Models of dry deposition predict deposition velocities as a function of particle size,
windspeed, and surface roughness. Because of their large surface area/ground area ratio,
vegetation surfaces receive the bulk of dry deposited particles over continental areas. Wet
and dry deposition account for the removal of over 400,000 t/year of the estimated 450,000
t/yr emissions (Nrlagu, 1979).
Lead enters soil as a moderately Insoluble lead sulfate and 1s immobilized by
complexation with hunlc and fulvlc acids. This Immobilization is a function of pH and the
concentration of humic substances. At low pH (~4) or low organic content (<5 percent),
Immobilization of lead in soil may be limited to a few hundred ^ig/g (Zimdahl and Skogerboe,
1977), but at 20 percent organic content and pH 6, 10,000 pg Pb/g soil may be found.
In natural waters, lead may precipitate as lead sulfate or carbonate, 'or it may form a
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Particles deposited by dry deposition on vegetation surfaces (leaves and bark) are
retained for the lifetime of the plant part. The particles are not easily washed off by rain
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PRELIMINARY DRAFT
7. ENVIRONMENTAL CONCENTRATIONS AND POTENTIAL PATHWAYS TO HUMAN EXPOSURE
7.1 INTRODUCTION
In general, typical levels of human lead exposure may be attributed to four components of
the human environment: food, inhaled air, dusts of various types, and drinking water. This
chapter presents Information on the ranges and temporal trends of concentrations in ambient
air, soil, and natural waters, and discusses the pathways from each source to food, inhaled
air, dust, and drinking water. The ultimate goal is to quantify the contribution of anthropo-
genic lead to each source and the contribution of each source to the total lead consumed by
humans. These sources and pathways of human lead exposure are diagrammed in Figure 7-1.
Chapters 5 and 6 discuss the emission, transport, and deposition of lead in ambient air.
Some information is also presented in Chapter 6 on the accumulation of lead 1n soil and on
plant surfaces. Because this accumulation is at the beginning of the human food chain, it is
critical to understand the relationship between this lead and lead in the human diet. It is
also important where possible to project temporal trends.
In this chapter, a baseline level of potential human exposure is determined for a normal
adult eating a typical diet and living in a non-urban community. This baseline exposure is
deemed to be unavoidable by any reasonable means. Beyond this level, additive exposure factor
s can be determined for other environments (e.g., urban, occupational, smelter communities),
for certain habits and activities (e.g., pica, smoking, drinking, and hobbies), and for varia-
tions due to age, sex, or socioeconomic status.
7.2 ENVIRONMENTAL CONCENTRATIONS
Quantifying human exposure to lead requires an understanding of ambient lead levels in
environmental media. Of particular importance are lead concentrations in ambient air, soil,
and surface or ground water. The following sections discuss environmental lead concentrations
1n each of these media in the context of anthropogenic vs. natural origin, and the contribu-
tion of each to potential human exposure.
7.2.1 Ambient Air
Ambient airborne lead concentrations may influence human exposure through direct inhala-
tion of lead-containing particles and through Ingestion of lead which has been deposited from
the air onto surfaces. Although a plethora of data on airborne lead is now available, our
understanding of the pathways to human exposure is far from complete because most ambient mea-
surements were not taken In conjunction with studies of the concentrations of lead in man or
in components of his food chain. However, that is the context in which these studies must now
PB7/A
7-1
7/14/83
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PRELIMINARY DRAFT
AUTO
EMISSIONS
CRUSTAL
WEATHERING
INDUSTRIAL
EMISSIONS
AMBIENT
AIR
SURFACE AND
GROUND WATER
SOIL
ANIMALS
PLANTS
INHALED
AIR
DRINKING
WATER
FOOD
DUSTS
MAN
Figure 7-1. Pathways of lead from the environment to human consumption. Heavy
arrows are those pathways discussed in greatest detail in this chapter.
PB7/A
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PRELIMINARY DRAFT
be interpreted to shed the most light possible on the concentrations likely to be encountered
in various environmental settings.
The most complete set of data on ambient air concentrations nay be extracted from the
National Filter Analysis Network (NFAN) and its predecessors (see Section 4.2,1), These data,
which are primarily for urban regions, have been supplemented with published data from rural
and remote regions of the United States. Because some stations in the network have been in'
place for about 15 years, information on temporal trends is available but sporadic. Ambient
air concentrations in the United States are comparable to other industrialized nations. In
remote regions of the world, air concentrations are two or three orders of magnitude lower,
lending credence to estimates of the concentration of natural lead in the atmosphere. In the
context of the NFAN data base, the conditions are considered which modify ambient air, as
measured by the monitoring networks, to air as inhaled by humans. Specifically, these
conditions are changes in particle size distributions, changes with vertical distance above
ground, and differences between indoor and outdoor concentrations.
7.2.1.1 Total Airborne Lead Concentrations. A thorough understanding of human exposure to
airborne lead requires detailed knowledge of spatial and temporal variations in ambient con-
centrations. The wide range of concentrations is apparent from Table 7-1, which summarizes
data obtained from numerous independent measurements. Concentrations vary from 0.000076 pg/m3
in remote areas to over 10 pg/m3 near sources such as smelters. Many of the remote areas are
far from human habitation and therefore do not reflect human exposure. However, a few of the
regions characterized by low lead concentrations are populated by individuals with primitive
lifestyles; these data provide baseline airborne lead data to which modern American lead expo-
sures can be compared. Examples include some of the data from South America and the data from
Nepal.
Urban, rural, and remote airborne lead concentrations in Table 7-1 suggest that human ex-
posure to lead has increased as the use of lead in inhabited areas has increased. This is
consistent with published results of retrospective human exposure studies. For example,
Ericson et al. (1979) have analyzed the teeth and bones of Peruvians buried 1600 years ago.
Based on their data, they estimate that the skeletons of present-day American and British
adults contain roughly 500 times the amount of lead which would occur naturally in the absence
of widespread anthropogenic lead emissions. Grandjean et al. (1979) and Shapiro et al. (1980)
report lead levels in teeth and bones of contemporary populations to be elevated 100-fold over
levels in ancient Nubians buried before 750 A.0. On the other hand, Barry and Connolly (1981)
report excessive lead concentrations in burled medieval English skeletons; one cannot discount
the possibility that the lead was absorbed into the skeletons from the surrounding soil.
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PRELIMINARY DRAFT
TABLE 7-1. ATMOSPHERIC LEAD IN URBAN, RURAL,
AND REMOTE AREAS OF THE WORLD
Location
Sampling period Lead conc. (jig/m3) Reference
Urban
TfTSii
New York
Boston
St. Louis
Houston
Chicago
Salt Lake City
Los Angeles
Ottowa
Toronto
Montreal
Berlin
Vienna
Zurich
Brussels
Turin
Rone
Paris
Rio de Janeiro
Rural
UiSTYork Bight
Fraainghatu, MA
Chadron, NE
United Kingdon
Italy
Belgium
Remote
White Mtn., CA
High Sierra, CA
Olympic Nat. Park, WA
Antarctica
South Pole
Thule, Greenland
Thule, Greenland
Prins Christian-
sund, Greenland
Dye 3, Greenland
Eniwetok, Pacific Ocean
Kuajung, Nepal
Bermuda
Spitsbergen
1974
1978-79
1978-79
1973
1978-79
1979
1974
1978-79
1975
1975
1975
1966-67
1970
1970
1978
1974-79
1972-73
1964
1972-73
1974
1972
1973-74
1972
1976-80
1978
1969-70
1976-77
1980
1971
1974
196S
1978-79
1978-79
1979
1979
1979
1973-75
1973-74
1.3
1.1
0.8
1.1
0.9
0.8
0.89
4
3
3
0
8
9
8
5
5
4.5
4.6
0.8
0.13
0.9
0.045
0.13
0.33
0.37
0.008
0.021
0022
0004
000076
0005
008
0.018
0.00015
0.00017
0.00086
0.0041
0.0058
HASL, 1975
see Table 7-3
see Table 7-3
see Table 7-3
see Table 7-3
see Table 7-3
HASL, 1975
see Table 7-3
NAPS, 1975
NAPS, 1975
NAPS, 1975
Blokker, 1972
Hartl and Resch, 1973
HSgger, 1973
Roels et al., 1980
Facchetti and Geiss, 1982
Colacino and Lavagnini, 1974
Blokker, 1972
Branquinho and Robinson, 1976
Duce et al., 1975
O'Brien et al., 1975
Strueepler, 1975
Cawse, 1974
Facchetti and Geiss, 1982
Roels et al. 1980
Chow et al., 1972
Elias and Davidson, 1980
Davidson et al., 1982
Duce, 1972
Maenhaut et al., 1979
Murozimi et al., 1969
Heidam, 1981
Heidam, 1981
Davidson et al., 1981c
Settle and Patterson, 1982
Davidson et al., 1981b
Duce et al., 1976
Larssen, 1977
Source: Updated fro* Nriaga, 1978
PB7/A
7-4
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PRELIMINARY DRAFT
The reBote area concentrations reported in Table 7-1 do not necessarily reflect natural,
prelndustrlal lead. Murozumi et al. (1969) and Ng and Patterson (1981) have measured a 200-
fold increase over the past 3000 years in the lead content of Greenland snow. In the opinion
of the authors, this lead originates in populated mid-latitude regions, and is transported
over thousands of kilometers through the atmosphere to the Arctic. All of the concentrations
fn Table 7-1, including values for remote areas, have been influenced by anthropogenic lead
emissions.
Studies referenced in Table 7-1 are limited in that the procedures for determining the
quality of the data are generally not reported. In contrast, the two principal airborne lead
data bases described 1n Section 4.2.1 include measurements subjected to documented quality as-
surance procedures. The U.S. Environmental Protection Agency's National Filter Analysis Net-
work (NFAN) provides comprehensive nationwide data on long-term trends. The second data base,
EPA's National Aerometrlc Data Bank, contains Information contributed by state and local
agencies, which Monitor compliance with the current ambient airborne standard for lead (1.5
Mg/m3 averaged over a calendar quarter) promulgated in 1978.
7.2.1.1.1 Distribution of air lead in the United States. Figure 7-2 categorizes the urban
sites with valid annual averages (4 valid quarters) into several annual average concentration
ranges (Akland, 1976; Shearer et al. 1972; U.S. Environmental Protection Agency, 1978, 1979;
Quarterly averages of lead from NFAN, 1982). Nearly all of the sites reported annual averages
below 1.0 tig/m*. Although the decreasing number of monitoring stations in service in recent
years could account for some of the shift in averages toward lower concentrations, trends at
Individual urban stations, discussed below, confirm the apparent national trend of decreasing
lead concentration.
The data from these networks show both the maximum quarterly average to reflect compli-
ance of the station to the ambient airborne standard (1.5 pg/m3), and quarterly averages to
show trends at a particular location. Valid quarterly averages must include at lease five
24-hour sampling periods evenly spaced throughout the quarter. The number of stations comply-
ing with the standard has increased, the quarterly averages have decreased, and the maximum
24-hour values appear to be smaller since 1977.
Table 7-2 provides cumulative frequency distributions of all quarterly lead concentra-
tions for urban NFAN stations (1st quarter = Jan-Mar, etc.). Samples collected by the NFAN
from 1970 through 1976 were combined for analysis into quarterly composites. Since 1977, the
24-hour samples have been analyzed individually and averaged arithmetically to determine
the quarterly average. These data show that the average lead concentration has dropped
markedly since 1977. An important factor in this evaluation is that the number of reporting
stations has also decreased since 1977. Stations may be removed from the network for several
PB7/A
7-5
7/14/83
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PRELIMINARY DRAFT
100
80
w
z
0
1
-J
$
P
~»
u.
O
L_
4-
196® 67 686970 71 7273 74 787877787980
(96) (1461 {IBS} (180) (130) (162) (72) 167)
YEAR
Figure 7-2. Percent of urban stations reporting indicated concentration interval.
PB7/A
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TABLE 7-2. CUMULATIVE FREQUENCY DISTRIBUTIONS OF URBAN AIR LEAD CONCENTRATIONS*
Percentile
Arithmetic
StdT
Geometric
5td7
Year
No. of
Station
Reports
10
30
50
70
90
95
99
Max.
Qtrly.
Avg
Mean
dev.
Mean
dev.
1970
797
0.47
0.75
1.05
1.37
2.01
2.59
4.14
5.83
1.19
0.80
0.99
1.80
1971
717
0.42
0.71
1.01
1.42
2.21
2.86
4.38
6.31
1.23
0.87
1.00
1.89
1972
708
0.46
0.72
0.97
1.25
1.93
2.57
3.69
6.88
1.13
0.78
0.93
1.87
1973
559
0.35
0.58
0.77
1.05
1.62
2.08
3.03
5.83
0.92
0.64
0.76
1.87
1974
594
0.36
0.57
0.75
1.00
1.61
1.97
3.16
4.09
0.89
0.57
0.75
1.80
1975
695
0.37
0.58
0.78
0.96
1.54
2.02
3.15
4.94
0.89
0.59
0.74
1.82
1976
670
0.37
0.58
0.74
0.96
1.41
1.72
3.07
4.54
0.85
0.55
0.72
1.80
1977
533
0.37
0.57
0.75
0.95
1.67
2.13
3.29
3.96
0.91
0.80
0.68
1.79
1978
282
0.27
0.43
0.57
0.74
1.19
1.49
2.40
3.85
0.68
0.64
0.50
1.87
1979
167
0.22
0.33
0.43
0.63
1.09
1.33
2.44
3.59
0.56
0.58
0.39
1.89
1980
220
0.14
0.21
0.30
0.38
0.55
0.66
0.84 1
1.06
0.32
0.27
0.24
1.88
*The data reported here are all valid quarterly averages reported fro* urban stations from 1970 to 1980,
in M
-------
PRELIMINARY DRAFT
reasons, the most common of which is that the locality has now achieved compliance status and
fewer monitoring stations are required. It 1s likely that none of the stations removed from
the network were in excess of 1.5 pg/n»3, and that most were below 1.0 MS/"3-
The summary percentiles and means for urban stations (Table 7-2) have decreased over the
period from 1970 to 1980, with most of the decrease occurring since 1977; the 1980 levels are
in the range of one-third to one-fourth of the values in 1970. The data from non-urban loca-
tions are given in Appendix 7A. While the composite nonurban lead concentrations are approxi-
mately one-seventh of the urban concentrations, they exhibit the same relative decrease over
the 1979-1980 period as the urban sites.
Long-term trends and seasonal variations in airborne lead levels at urban sites can be
seen in Figure 7-3. The 10th, 50th, and 90th percentile concentrations are graphed, using
quarterly composite and quarterly average data from an original group of 92 urban stations
(1965-1974) updated with data for 1975 through 1980. Note that maximum lead concentrations
typically occur in the winter, while minima occur in the summer. In contrast, automotive
emissions of lead would be expected to be greater in the summer for two reasons: (1) gasoline
usage is higher in the summer, and (2) lead content is raised in summer gasolines to replace
some of the more volatile high-octane components that cannot be used in summertime gasolines.
The effect is apparently caused by the seasonal pattern of lower dispersion capacity in
winter, higher capacity in summer.
Figure 7-3 also clearly portrays the significant decrease in airborne le^d levels over
the past decade. This trend is attributed to the decreasing lead content of regular and pre-
mium gasoline, and to the increasing usage of unleaded gasoline. The close parallel between
these two parameters is discussed in detail in Chapter 5. (See Figure 5-4 and Table 5-6.)
The decrease in lead concentrations, particularly in 1979 and 1980, was not caused by the
disappearance from the network of monitoring sites with characteristically high concentra-
tions; the quarterly values for sites in six cities representing the east coast, the central,
and the western sections of the country (Figure 7-4) indicate that the decrease is widespread
and real.
Table 7-3 shows lead concentrations in the atmospheres of several major metropolitan
areas of epidemiological Interest. Some of the data presented do not meet the stringent re-
quirements for quarterly averages and occasionally there have been changes in site location or
sampling methodology. Nevertheless, the data are the best available for reporting the history
of lead contamination in these specific urban atmospheres. Further discussions of these data
appear in Chapter 11.
PB7/A
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TABLE 7-3. AIR LEAD CONCENTRATIONS IN MAJOR METROPOLITAN AREAS (jig/m3) (quarterly averages)
Boston
Hew York
Phi la. Wash.
Detroit
Chicago
Houston
Oat tas/Ft.Worth
Los Angeles
m
NY
PA DC
HI
IL
IX
IX
CA
Station
Type
1
1
1 4 1
1
1 2 3
1
4
1
2
4
1
2
Year
Quarter
1970
1
0.8
1.2
0.9
1.2
1.8
3.8
5.7
3.2
2
1.5
0.9
1.4
f.O
2.3
3.5
2.2
3
1.2
1.9
1.4
1.9
2.8
5.1
3.3
4
1.2
1.4
1.2
1.3
2.5
3.7
3.9
1.9
1971
I
1.6
1.1
1.0
1.9
3.4
6.0
2
0.7
1.8
1.3
1.8
1.6
1.8
2.9
3
1.3
1.6
1.7
2.5
3.3
4
1.7
2.1
2.2
2.7
2.7
6.3
1972
1
1.0
0.9
1.7
2.3
3.4
3.1
2
0.6
1.3
1.2
1.0
1.8
2.0
1.6
3
2.5.
1.0
0.9
2.2
2.6
1.5
4
1.1
1.1
2.3
2.8
4.7
2.1
1973
1
0.8
2.9
1.9
2.7
1.6
2
1.8
1.3
2.0
2.5
3
0.6
1.3
1.7
2.7
4
0.9
1.7
1.9
1974
1
0.5
0.5
1.8
1.3
1.9
1.6
2
0.9
1.1
2.0
0.6a
1.4
0.2a
2.0
1.7
3
1.0
0.9
0.9
1.8
0.6
2.8
0.4
1.4
1.9
4
0.9
0.9
2.6
0.5
3.3
0.6
3.2
2.6
1975
1
1.2
0.8
' 1.1
0.8
2.1a
0.7
2.9
0.3
1.7
2
0.6a
0.8
0.7
1.7
0.7
2.3
0.3
1.2
1.2
3
1.0a
1.0
1.2
2.1
0.6
3.0
0.4
1.9
1.7
4
0.9a
1.1
1.2
2.4
1.1
2.9
0.5
0.3
3.2
2.2
-------
TABLE 7-3. (continued)
Boston
New York
Chi la.
Wash.
Detroit
Chicayo
Houston
Dallas/Ft.
Worth
Los Anqeles
MA
NV
DC
Ml
1L
IK
TX
CA
Station
Type
1
1
1
4
1
1
1
2
3
1 4
1
2
1
1
2
¥#ar
Quarter
1976
1
0.8a 0.5
0.7a
0.3
0.2
2
1.2a
0.7a 0.5
0.7
0.3
0.4
3
.
1.4
1.1 0.7
1.1a
0.3
0.3
4
0.4a
4.1
3.0
1977
1
1.3
1.0
1.2
1.1
2.3
3.3
2.4
2
1.6
0.8
0.9
0.3a 0.2
1.2
0.2
0.2
1.7
1.4
3
0.6a
1.4
0.9
0.9a
1.0
0.8 0.3
1.1
0.2
0.2
1.8
1.6
4
0.7
1.3
1.0
2.1
1.3 0.7
1.6a
0.5
0.5
3.8
2.9
1978
1
0.8
1.2
0.8
2.2
1.0 0.5
1.7a
0.4
0.3
2.2a
1.6
2
1.0a
1.1
0.7
1.1
0.8 0.4
1.1
0.4
0.3
3
0.9
1.4
0.7
1.1
0.8 0.5
1.3
0.4
0.3
1.6
4
1.3
1.3
1.6
1.2
3.3
1.7 0.9
1.7
0.5
0.6
1.9
1979
1
1.0
1.0a
1.1
0.7
1.8
0.9 0.4
1.2a
0.4
0.4
1.5
2
0.4
0.9
1.2
0.6
1.3
0.7
0.9
0.8
0.8 0.4
0.6a
0.2
0.3
0.9
3
0.6
1.0
0.6
1.6
0.5
0.6
0.8
0.5a 0.6a
1.1a
0.4
0.6
1.0a
4
0.8a
1.2
0.8
1.9
0.7a 0.5
0.5a
0.3
0.4
0.6a
1980
1
0.9a
0.7
0.4
0.3
0.4
0.3
0.3
0.6a 0.3
0.3a
0.3
0.2
0.7
1.1
2
0.4
0.4
0.3
0.7
0.4
0.6
0.3a 0.3a
0.6a
0.1
0.2
0.8
3
0.5
0.7
0.4
0.3
1.0
0.5
0.5
0.2
0.3
0.1
0.1
1.1a
1.0
4
0.6
0.7
O.S
0.4a
0.5
0.4
0.4
0.4
0.4
0.3
0.3
1.7
1981
1
0.4
0.5
0.4a
0.3
0.2
0.3
0.2
0.7 0.5
0.6
0.3
0.3
1.3
1.0
2
0.3
0.4
0.3
0.3
0.4
0.3
0.3
0.2 0.2
0.3
0.1
0.2
0.7
0.7
3
0.4
0.2
0.3
0.3
0.3
0.2
0.5 0.3
0.2
0.3
0.8
0.8
4
0.4
0.3
0.3a
0.4
0.2a 0.3
0.8 1.0a
0.3
0.4
1.3
1.1
1982
1
0.3
0.4
0.3
0.3
0.8
0.7
2
0.5
0.3
0.2
0.4
0.3
0.5
3
1.0
o.s
0.3
0.3
0.3
0.2
O.S
4
0.8a
0.4
0.4
0.3
0.3
1.1
0.6
Station type: I. center city CMwercial
2. center city residential
3. center city industrial
4. suburban residential
a: less than required number of 24-hour sa*pling periods to Beet composite criteria
-------
PRELIMINARY DRAFT
•0th PERCENTILE
60th PERCENTILE
86 68 87 88 88 70 71 72 73 74 76 78 77 78 78 80
YEAR
Figure 7-3. Seasonal patterns and trends in quarterly average urban lead concentrations.
7.2.1.1.2 Global distributions of air lead. Other industrialized nations have maintained
networks for monitoring atmospheric lead. For example, Kretzschnwr et al. (1980) reported
trends from 1972 to 1977 in a 15-station network ih Belgium. Annual averages ranged from 0.16
Mg/m at rural sites to 1.2 jjg/rn3 near the center of Antwerp. All urban areas showed a
maximum near the,center of the city, with lead concentrations decreasing outward. The rural
background levels appeared to range from 0.1 to 0.3 pg/m3. Representative data from other
nations appear in Table 7-1.
7.2.1.1.3 Natural concentrations of lead in air. There are no direct measurements of pre-
historic natural concentrations of lead in air. Air lead concentrations which existed in pre-
historic times must be inferred from available data. Table 7-1 lists several values for re-
mote areas of the world, the lowest of which is 0.000076 yg/ma at the South Pole (Maenhaut et
al., 1979). Two other reports show comparable values: 0.00017 jig/m8 at Eniwetok in the
Pacific Ocean (Settle and Patterson, 1982) and 0.00015 at Dye 3 in Greenland (Davidson et al.,
1981a). Since each of these studies reported some anthropogenic Influence, it may be assumed
that natural lead concentrations are somewhat lower than these measured values.
PB7/A
7-11
7/1/83
-------
z
o
F=
IK
O
z
o
o
i i i i
TUCSON. AZ
1.4
1.2
1.0
0J
0.6
0.4
0.2
1.8
1.6
1.4
1J
1.0
0.8
0.6
0.4
02
WORCHESTER, MA
NEWARK. NJ
I I I I I
I I I I I
DES MOINES, IA
AKRON, OH
I I I I I
PBJ/k
1978 76 77 78 78 80 1975 78 77 78 79 80
YEAR
Figure 74. Time trends in ambient air lead at selected urban sites.
7-12 7/1/83
-------
PRELIMINARY DRAFT
Another approach to determining natural concentrations 1s to estimate global emissions
from natural sources. Nriagu (1979) estimated emissions at 24.5 x 10® kg/yr, whereas Settle
and Patterson (1980) estimated a lower value of 2 x 10® kg/yr. An average troposheric volume,
to which surface generated particles are generally confined, is about 2.55 x 1010n3. Assuming
a residence time of 10 days (see Section 6.3), natural lead emissions during this time would
be 6.7 x 1014 pg. The air concentrations would be 0.000263 using the values of Nriagu (1979)
or 0.0000214 pg/m3 using the data of Settle and Patterson (1980). It seems likely that the
concentration of natural lead in the atmosphere is between 0.00002 and 0.00007 pg/m3. A value
of 0.00005 pg/m3 will be used for calculations regarding the contribution of natural air lead
to total human uptake in Section 7.3.1.
7.2.1.2 Compliance with the 1978 Air Quality Standard. Table 7-4 lists stations operated by
state and local agencies where one or more quarterly averages exceeded 1.0 pg/m3 or the cur-
rent standard of 1.5 pg/m3 in 1979 or 1980. A portion of each agency's compliance monitoring
network consists of monitors sited in areas expected to yield high concentrations associated
with identifiable sources. In the case of lead, these locations are most likely to be near
stationary point sources such as smelters or refineries, and near routes of high traffic den-
sity. Both situations are represented in Table 7-4; e.g., the Idaho data reflect predominant-
ly stationary source emissions, whereas the Washington, O.C. data reflect predominantly
vehicular emissions.
Table 7-5 summarizes the maximum quarter lead values for those stations reporting 4 valid
quarters in 1979, 1980, and 1981, grouped according to principal exposure orientation or in-
fluence—population, stationary source, or background. The sites located near stationary
sources clearly dominate the concentrations over 2.0 pg/m3; however, new siting guidelines,
discussed in Section 7.2.1.3.2, will probably effect some Increase in the upper end of the
distribution of values from population-oriented sites by adding sites closer to traffic emis-
sions.
The effect of the 1978 National Ambient Air Quality Standard for Lead has been to reduce
the air concentration of lead in major urban areas. Similar trends may also be seen in urban
areas of lower population density (Figure 7-4). Continuous monitoring at non-urban stations
has been insufficient to show a trend at more than a few locations.
7.2.1.3 Changes in Air Lead Prior to Human Uptake. There are many factors which can cause
differences between the concentration of lead measured at a monitoring station and the actual
inhalation of air by humans. The following sections show that air lead concentrations usually
decrease with vertical and horizontal distance from emission sources, and are generally lower
indoors than outdoors. A person working on the fifth floor of an office building would be ex-
posed to less lead than a person standing on a curb at street level. The following dis-
cussions will describe how these differences can affect individual exposures in particular
circumstances.
PB7/A 7-13 7/14/83
-------
TABLE 7-4. STATIONS WITH AIR LEAD CONCENTRATIONS GREATER THAN 1.0 mo/b3
Data are listed from all stations, urban and rural, reporting valid quarterly averages greater than 1.0
Mg/n3. Some stations have not yet reported data for 1981.
1979
Max
1980
Max
1981
Max
No. of Quarters
Qtrly
No. of Quarters
Qtrly
No of Quarters
Qtrly
Station #
>1.0
>1.5
Ave
>1.0
>1.5
Ave
>1.0
>1.5
Ave
Troy, AL
(003)
2
2
2.78
2
0
1.13
2
2
4.32
Glendale, AZ
(001)
1
0
1.06
Phoenix, AZ
(002A)
1
1
1.54
2
0
1.29
1
0
1.17
M «
(002G)
2
2.59
2
0
1.49
2
0
1.39
II II
(004)
2
0
1,48
1
0
1.04
tt li
(013)
2
1.55
1
0
1.06
Scottsdale, AI
(003)
2
0
1.41
1
0
1.13
1
0
1.08
Tucson, AZ
(009)
1
0
1.18
Nogales, AZ
(004)
1
0
1.10
Los Angeles, CA
(001)
1
1
1.51
2
0
1.43
Anahein, CA
(001)
1
0
1.11
Adaas Co, CO
(001)
2
1
1.77
Arapahoe Co, CO
(001)
1
0
1.10
Arvada, CO
(001)
1
1
1.60
Brighton, CO
(001)
1
0
1.17
Colorado Springs,CO
(004)
1
0
1.37
Denver, CO
(001)
2
1 "
1.70
H II
(002)
4
3
3.47
2
1
1.53
11 II
(003)
3
1
2.13
1
0
1.03
11 II
(009)
1
1
1.57
2
0
1.23
II II
(010)
2
1
1.67
tl II
(012)
2
1
1.67
1
0
1.10
Englewood, CO
(001)
1
1
1.80
Garfield, CO
(001)
1
0
1.20
Grand Junction, CO
(010)
2
1
1.53
1
0
1.27
Longnont, CO
(001)
2
0
1.07
Pueblo, CO
(001)
1
0
1.03
H II
(003)
1
0
1.03
Routt Co, CO
(003)
1
0
1.33
New Haven, CT
(123)
3
1.57
Waterbury, CT
(123)
2
0
1.41
Wilmington, OE
(002)
2
0
1.21
-------
TABLE 7-4. (continued)
1979 Max 1980 Max 1981 Max
No. of Quarters Qtrly No. of Quarters Qtrly No of Quarters Qtrly
Station # >1.0 >1.5 Ave >1.0 >1.5 Ave >1.0 >1.5 Ave
Washington, DC
(005)
1
0
1.49
II ti
(007)
4
1.89
II II
(008)
1
1
1.90
II II
(011)
2
0
1.44
ll ta
(015)
2
0
1.06
it ll
(017)
1
0
1.45
Dade Co, FL
(020)
1
0
1.16
Miaai, FL
(016)
3
0
1.46
2
0
1.10
Perrine, FL
(002)
1
0
1.01
Hillsborough, FL
(082)
2
0
1.31
1
0
1.09
Taapa, FL
(043)
3
1.60
1
0
1.07
Boise, ID
(003)
1
0
1.01
Kellogg, 10
(004)
4
9.02
2
6.88
M II
(006)
4
4
8.25
4
4
8.72
4
4
6.67
Shoshone Co, ID
(015)
2
0
1.21
M II
(016)
1
1
2.27
1
0
1.02
II II
(017)
4
4.57
3
3.33
2
2
1.54
U II
(020)
2
4.11
2
2.15
1
0
1.49
II II
(021)
4
4
13.54
4
4
13.67
4
4
11.82
II II
(027)
4
10.81
3
7.18
Chicago, IL
(022)
1
0
1.02
N II
(030)
1
0
1.06
It II
(005)
1
0
1.05
H M
(036)
1
0
1.02
II II
(037)
1
0
1.14
Cicero, IL
(001)
1
0
1.00
Elgin, IL
(004)
1
1
1.95
Granite City, IL
(007)
1
0
1.04
II »
(009)
4
0
1.15
tt H
(010)
4
4
3.17
3
2
2.97
4
3
7.27
II II
(011)
4
0
1.33
1
0
1.43
1
0
1.13
Jeffersonville, IN
(001)
3
0
1.38
East Chicago, IL
(001)
2
2.19
II 11
(003)
2
0
1.42
u u
(004)
1
1
1.67
M II
(006)
2
0
1.34
1
0
1.04
-------
TABLE 7-4. (continued)
1979 Max 1980 Max 1981 Max
No. of Quarters Qtrly Ho. of Quarters Qtrly No of Quarters Qtrly
Station# >1.0 >1.5 Ave >1.0 >1.5 Ave >1.0 >1.5 Ave
Hammond, IN
(004)
2
0
1.18
11 II
(006)
1
0
1.46
Indianapolis, IN
(030)
1
0
1.16
Des Moines, IA
(051)
1
0
1.30
Buechel, KY
(001)
1
0
1.41
Covington, KY
(001)
2
0
1.12
II II
(008)
1
0
1.16
Greenup Co, KY
(003)
1
0
1.42
Jefferson Co, Ky
(029)
1
0
1.05
1
1
1.78
Louisville, KY
(004)
1
0
1.01
1
1
2.41
11 It
(009)
1
1
1.75
fl II
(019)
1
1
1.59
U II
(020)
1
1
2.52
11 If
(021)
1
0
1.29
1
1
1.42
II II
(028)
1
0
1.06
Newport, KY
(002)
1
0
1.06
Okolona, KY
(001)
1
1
1.51
2
1
2.31
Paducha, KY
(004)
1
0
1.41
l« II
(020)
1
0
1.22
St. Matthews, KY
(004)
1
0
1.20
1
1
1.83
Shively, KY
(002)
1
1
1.56
Baton Rouge, LA
(002)
1
1
1.57
Portland, ME
(009)
2
0
1.02
Anne Arundel Co,
MO (001)
1
0
1.27
II II
(003)
2
0
1.45
Baltimore, MO
(001)
2
0
1.06
II II
(006)
1
0
1.09
II U
(008)
1
0
1.24
II II
(009)
1
0
1.08
14 II
(018)
2
0
1.12
Cheverly, MO
(004)
4
1
1.51
Essex, MD
(001)
2
0
1.15
Hyattsville, MD
(001)
2
0
1.18
Springfield, MA
(002)
1
1
1.68
1
0
1.04
Boston, MA
(012)
1
0
1.01
-------
TABLE 7-4. (continued)
1979
Max
1980
Max
1981
Max
No.
of Quarters
Qtrly
No. of Quarters
Qtrly
No of Quarters
Qtrly
Station # >1.C
1 >1.5
Ave
>1.0
>1.5
Ave
>1.0
>1.5
Ave
Minneapolis, MN
(027)
1
1
2.44
II II
(055)
3
2.41
3
1
1.52
Richfield, MN
(004)
4
1.95
2
0
1.18
St. Louis Park, MN
(007)
2
2.87
4
3.04
St. Paul, MN
(031)
1
0
1.04
II II
(038
1
0
1.36
3
1.82
2
2
3.11
Lewis & Clark Co, NT (002)
4
4.19
4
2.75
2
2
3.19
II II
(008)
1
0
1.19
Omaha, NE
(034)
1
0
1.08
Las Vegas, NV
(001)
1
0
1.15
Newark, NJ
(001)
1
0
1.17
Perth Aaboy, NJ
(001)
1
0
1.08
Paterson, NJ
(001)
1
0
1.42
Elizabeth, NJ
(002)
1
0
1.16
Yonkers, NY
(001)
1
0
1.08
Cincinnati, OH
(001)
1
0
1.15
Laurel dale, PA
(717)
4
3.30
2
1.86
4
3
2.18
Reading, PA
(712)
1
0
1.11
E.Coneaaugh, PA
(804)
3
0
1.28
Throop, PA
(019)
3
0
1.13
Lancaster City, PA
(315)
1
0
1.18
New Castle, PA
(015)
1
0
1.01
Montgomery Co, PA
(103)
1
0
1.23
Pottstown, PA
(101)
1
0
1.16
Phila., PA
(026)
3
0
1.21
II II
(028)
4
2.71
3
0
1.26
1
0
1.30
« ii
(031)
2
0
1.29
H «i
(038)
1
0
1.06
Guaynabo Co, PR
(001)
2
1.60
1
0
1.06
1
0
1.02
Ponce, PR
(002)
1
0
1.08
San Juan Co., PR
(003)
4
3.59
E.Providence, RI
(008)
2
0
1.10
Providence, RI
(007)
4
1.92
2
0
1.16
il II
(015)
1
0
1.34
Greenville, SC
(001)
2
0
1.38
-------
TABLE 7-4, (continued)
1979 Max 1980 Max 1981 Max
Mo. of Quarters Qtrly No, of Quarters Qtrly No of Quarters Qtrly
Station# >1.0 >1.5 Ave >1.0 >1.5 Ave >1.0 >1.5 Ave
Nashville/Dav1dson,
TN
(006)
1
0
1.05
San Antonio, TX
(034)
1
0
1.23
Dallas, TX
(018)
1
1
1.59
II II
(029)
1
0
1.07
il li
(035)
1
0
1.12
U ft*
(046)
1
0
1.22
II K ^
(049)
1
0
1.01
U II
(050)
2
0
1.13
El Paso, TX
(002A)
1
1
1,90
II U
(002F)
1
1
1.90
II II
(002G)
4
2.60
II «
(018)
2
1.91
ii n
(021)
1
0
1.02
II u
(022)
2
1.84
ii u
(023)
2
2.12
ii ii
(027)
2
2.15
it ii
(028)
n w
(030)
1
0
1.02
ii ai
(031)
1
1
2.47
ii ii
(033)
1
1
1.97
Houston, TX
(001)
2
0
1.35
11 Ii
(002)
2
0
1.39
II U
(037)
1
0
1.26
it y
(049)
3
0
1.13
Ft. Worth, TX
(003)
2
0
1.14
Seattle, VA
(057)
1
0
1.36
Tacowa, MA
(004)
1
0
1.06
Charleston, WV
(001)
1
0
1.09
2.12
1.79
2
1
1.74
1.16
1.75
1.96
-------
PRELIMINARY DRAFT,
TABLE 7-5. DISTRIBUTION OF AIR LEAD CONCENTRATIONS BY TYPE OF SITE
Concentration ranges (pg/m3)
Site-type
S.5
>.5
Sl.O
>1.0
SI. 5
>1.5
£2.0
>2.0
Total no.of
site-years
Population
300
173
46
7
5
531
Stationary
source
50
12
10
2
21
95
Background
21
0
0
0
0
21
Total
(site-years)
371
185
56
9
26
647
Percent of sites
in concentration
range
57%
29%
9%
1%
4%
100%
Data are the number of site years during 1979-81 falling within the designated quarterly aver-
age concentration range. To be Included, a site year nust have four valid quarters of data.
7,2.1.3.1 Airborne particle size distributions. The effects of airborne lead on human health
and welfare depend upon the sizes of the lead-containing particles. As discussed 1n Chapter
6, large particles are removed relatively quickly from the atmosphere by dry and wet deposi-
tion processes. Particles with diameter smaller than a few micrometers tend to renaln
airborne for long periods (see Section 6.3.1).
Figure 7-5 summarizes airborne lead particle size data fro# the literature. Minimum and
nax 1 mum aerodynamic particle diameters of 0.05 pat and 25 >»>, respectively, have been assumed
unless otherwise specified 1n the original reference. Note that most of the airborne lead
nass is associated with small particles. There 1s also a distinct peak in the upper end of
many of the distributions. Two separate categories of sources are responsible for these dis-
tributions: the small particles result from nucleation of vapor phase lead emissions (pre-
dominantly automotive), while the larger particles represent primary aerosol emitted from com-
bustion or from mechanical processes (such as soil erosion, abrasion of metal products, re-
suspension of automobile tailpipe deposits, and flaking of paint).
Information associated with each in the distributions in Figure 7-5 may be found 1n Table
7A-1 of Appendix 7A. The first six distributions were obtained by an EPA cascade Impactor
network established in several cities during the calendar year 1970 (Lee et al., 1972). These
PB7/A
7-19
7/14/83
-------
PRELIMINARY DRAFT
distributions represent the most extensive size distribution data base available. However,
the impactors were operated at excessive air flow rates that most likely resulted in particle
bounceoff, biasing the data toward smaller particles (Dzubay et al., 1976). Many of the later
distributions, although obtained by independent investigators with unknown quality control,
were collected using techniques which minimize particle bounceoff and hence may be more reli-
able. It is important to note that a few of the distributions were obtained without backup
filters that capture the smallest particles. These distributions are likely to be inaccurate,
since an appreciable fraction of the airborne lead mass was probably not sampled. The distri-
butions of Figure 7-5 have been used with published lung deposition data to estimate the frac-
tion of inhaled airborne lead deposited in the human respiratory system (see Chapter 10).
7.2.1.3.2 Vertical gradients and siting guidelines. New guidelines for placing ambient air
lead monitors went into effect in July, 1981 (F.R., 1981). "Microscale" sites, placed between
5 and 15 meters from thoroughfares and 2 to 7 meters above the ground, are prescribed, but
until now few monitors have been located that close to heavily traveled roadways. Many of
these microscale sites might be expected to show higher lead concentrations than that measured
at nearby middlescale urban sites, due to vertical gradients in lead concentrations near the
source. One study (PEDCo, 1981) gives limited insight into the relationship between a micro-
scale location and locations further from a roadway. The data in Table 7-6 summarize total
suspended particulates and particulate lead concentrations in samples collected in Cincinnati,
Ohio, on 21 consecutive days in April and May, 1980, adjacent to a 58,500 vehicles-per-day
expressway connector. Simple interpolation indicates that a microscale monitor as close as 5
meters from the roadway and 2 meters abo.ve the ground would record concentrations some 20 per-
cent higher than those at a "middle scale" site 21.4 meters from the roadway. On the other
hand, these data also indicate that although lead concentrations very close to the roadway
(2.8 m setback) are quite dependent on the height of the sampler, the averages at the three
selected heights converge rapidly with increasing distance from the roadway. In fact, the
average lead concentration (1.07 ng/ms) for the one monitor (6.3 a height, 7.1 m setback) that
satisfies the microscale site definition proves not to be significantly different from the
averages for its two companions at 7.1 n, or from the averages for any of the three monitors
at the 21.4 m setback. It also appears that distance from the source, whether vertical or
horizontal, can be the primary determining factor for changes in air lead concentrations. At
7,1 ¦ from the highway, the 1.1 and 6.3 m samplers would be about 7 and 11 meters from the
road surface. The values at these vertical distances are only slightly lower than the
corresponding values for comparable horizontal distances.
PB7/A
7-20
7/14/83
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PRELIMINARY ORAFT
140
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0
0.01 O.t 1 10 0.01 0.1 1 19 0.01 0.1 1 10 0.01 0,1 1 10 0J1 0.1 1 10
<*p,m
Figure 7-6. Airborne mass size distributions for lead taken from the literature. AC represents
tha airborne lead concentration in each siza range, Cj is the total airborne lead concentra-
tion In all size ranges, and dp Is the aerodynamic particle diameter. A density of 6 g/cm* for
lead-containing particles has been used to convert aerodynamic to physical diameter when
applying the lower end of the lung deposition curves of Figures 7-3 through 7-6.
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PB7/A
7-21
7/1/83
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PRELIMINARY DRAFT
TABLE 7-6. VERTICAL DISTRIBUTION Of LEAD CONCENTRATIONS
Setback
distance
Cm)
Height
Cm)
Effective1
distance
from
source
(m)
Air lead
cone,
(Mfl/"»3)
Ratio to
source
Kansas City
east of road
3.0*
6.1
6.4
1,7
0.85
1.5
3.2
2.0
S
Kansas City
west of road
3.0*
6.1
6.4
1.5
0.88
1.5
3.2
1.7
S
Cincinnati
east of road
3.0*
6.1
6.4
0.9
0.64
1.5
3,2
1.4
S
Cincinnati
west of road
3.0*
6.1
6.4
0.6
0.75
1.5
3.2
0.8
S
Cincinnati
2.8
10.5
10.4
0.81
0.61
6.3
6.4
0.96
0.72
1.1
2.9
1.33
S
Cincinnati
7.1
10.5
12.3
0.93
0,69
6.3
3,2
1.07
0.80
1.1
7.1
1.16
0.87
Ci nci nnati
21.4
10.5
23.6
0.90
0.68
6.3
22.2
0.97
0.73
1.1
21.4
1.01
0.77
S = Station closest to source used to calculate ratio.
Effective distance was calculated assuming the source was the edge of the roadway at a height
of 0.1 m.
"Assumed setback distance of 3.0 m.
Other urban locations around the country with their own characteristic wind flow patterns
and complex settings, such as Multiple roadways, nay produce situations where the nicroscale
site does not record the highest concentrations. Collectively, however, the addition of these
¦icroscale sites to the nation's networks can be expected to shift the distribution of
reported quarterly averages toward higher values. This shift will result from the change in
composition of the networks and is a separate phenomenon from downward trend at long estab-
lished sites described above, reflecting the decrease in lead additives used in gasoline.
PB7/A
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7/14/83
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PRELIMINARY ORAFT
Two other studies show that lead concentrations decrease with vertical distance fro* the
source. PEOCo-Environmental (1977) measured lead concentrations at heights of 1.5 and 6.1 m
at sites in Kansas City, MO and Cincinnati, OH. The sampling sites in Kansas City were des-
cribed as unsheltered, unbiased by local pollution influences, and not immediately surrounded
by large buildings. The Cincinnati study was conducted in a primarily residential area with
one commercial street. Samplers were operated for 24-hour periods; however, a few 12-hour
samples were collected from 8 AM to 8 PM. Data were obtained in Kansas City on 35 days and 1n
Cincinnati on 33 days. The range and average values reported are shown in Table 7-7. In all
cases except two, the measured concentrations were greater at 1.5 meters than at 6.1 meters.
Note that the difference between the east side and west side of the street was approximately
the same as the difference between 1.5 m and 6.1m in height.
Sinn (1980) investigated airborne lead concentrations at heights of 3 and 20 m above a
road in Frankfurt, Germany. Measurements conducted in December 1975, December 1976, and Janu-
ary 1978 gave monthly mean values of 3.18, 1.04, and 0.66 |jg/m3, respectively, at 3 m. The
corresponding values at 20 m were 0.59, 0.38, and 0.31 pg/m3, showing a substantial reduction
at this height. The decrease in concentration over the 2-year period was attributed to a de-
crease in the permissible lead content of gasoline from 0.4 to 0.15 g/liter beginning in Janu-
ary 1976.
Two reports show no relationship between air concentration and vertical distance. From
August 1975 to July 1976, Barltrop and Strehlow (1976) conducted an air sampling program in
London at a proposed nursery site under an elevated motorway. The height of the motorway was
9.3 m. Air samplers were operated at five to seven sites during the period from Monday to
Friday, 8 AM to 6 PM, for one year. The maximum individual value observed was 18 pg/m*. The
12 month mean ranged from 1.35 pg/m® to 1.51 jig/ms, with standard deviations of 0.91 and 0.66,
respectively. The authors reported that the airborne concentrations were independent of height
from ground level up to 7 n.
Ter Haar (1979) measured airborne lead at several heights above the ground, using
samplers positioned 6 m from a heavily traveled road in Oetroit. A total of nine 8-hour day-
time samples were collected. The overall average airborne lead concentrations at heights of
0.3, 0.9, 1.5, and 3.0 m were 4.2, 4.8, 4.7, and 4.6 Hfl/«*» respectively, indicating a uniform
concentration over this range of heights at the measurement site. It should be noted that at
any one height, the concentration varied by as much as a factor of 10 from one day to the
next; the importance of simultaneous sampling when attempting to measure gradients is clearly
demonstrated. '
Data that show variations with vertical distance reflect the strong influence of the geo-
metry of the boundary layer, wind, and atmospheric stability conditions on the vertical gradi-
ent of lead resulting from automobile emissions. The variability of concentration with height
PB7/A 7-23 7/14/83
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PRELIMINARY DRAFT
is further complicated by the higher emission elevation of smokestacks. Concentrations
measured fro* sampling stations on the roofs of buildings several stories high may not reflect
actual human exposure conditions, but neither would a single sampling station located at
ground level in a building complex. The height variation in concentration resulting from
vertical diffusion of automobile emissions is likely to be small compared to temporal and
spatial variations resulting from surface geometry, wind, and atmospheric conditions. Our
understanding of the complex factors affecting the vertical distribution of airborne lead is
extremely limited, but the data of Table 7-6 indicate that air lead concentrations are pri-
marily a function of distance from the source, whether vertical or horizontal.
7.2.1.3.3 Indoor/outdoor relationships. Because people spend much of their time Indoors, am-
bient air data may not accurately indicate actual exposure to airborne lead. Table 7-7 sum-
marizes the results of several indoor/outdpor airborne lead studies. In nearly all cases, the
indoor concentration is substantially lower than the corresponding value outdoors; the only
indoor/outdoor ratio exceeding unity is for a high-rise apartment building, where air taken in
near street level 1s rapidly distributed through the building air circulation system. Some of
the studies in Table 7-7 show smaller indoor/outdoor ratios during the winter, when windows
and doors are tightly closed. Overall, the data suggest indoor/outdoor ratios of 0.6 to 0.8
are typical for airborne lead in houses without air conditioning. Ratios in air conditioned
houses are expected to be in the range of 0.3 to 0.5 (Yocum, 1982).
The available data Imply that virtually all airborne lead found Indoors is associated
with material transported from the outside. Because of the complexity of factors affecting
infiltration of air into buildings, however, it is difficult to predict accurately indoor lead
concentrations based on outdoor levels. Even detailed knowledge of indoor and outdoor air-
borne lead concentrations at fixed locations may still be insufficient to assess human expo-
sure to airborne lead. The study of Tosteson et al. (1982) in Table 7-7 Included measurement
of airborne lead concentrations using personal exposure monitors carried by individuals going
about their day-to-day activities. In contrast to the lead concentrations of 0.092 and 0.12
Mfl/m3 at fixed locations, the average personal exposure was 0.16 ng/m3. The authors suggest
this indicates an inadequacy of using fixed monitors at either indoor or outdoor locations to
assess exposure.
7.2.2 Lead in Soil
Much of the lead in the atmosphere 1s transferred to terrestrial surfaces where it 1s
eventually passed to the upper layer of the soil surface. The mechanisms which determine the
transfer rate of lead to soil are described in Section 6.4.1 and the transformation of lead in
PB7/A
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7/14/83
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PRELIMINARY DRAFT
profile. It is assumed that particles deposited directly on the roadway are washed to the
edge of the pavement, but do not migrate beyond the shoulder.
Near primary and secondary smelters, lead in soil decreases exponentially within a 5 to
10 km zone around the smelter complex. Soil lead contamination varies with the smelter emis-
sion rate, length of time the smelter has been in operation, prevailing windspeed and direc-
tion, regional climatic conditions, and local topography (Roberts, 1975).
little and Martin (1972) observed decreases from 125 to 10 pg/g in a 6 km zone around a
smelting complex in Great Britain; all of the excess lead was in the upper 6 cm of the soil
profile. Roberts (1975) reported soil lead between 15,000 and 20,000 |jg/g near a smelter in
Toronto. Kerin (1975) found 5,000 to 9,000 pg/g adjacent to a Yugoslavian smelter; the con-
tamination zone was 7 km in radius. Ragaini et al. (1977) observed 7900 pg/g near a smelter
in Kellogg, Idaho; they also observed a 100-fold decrease at a depth of 20 cm in the soil pro-
file. Palmer and Kucera (1980) observed soil lead in excess of 60,000 pg/g near two smelters
in Missouri, decreasing to 10 pg/g at 10 km.
Urban soils may be contaminated from a variety of atmospheric and non-atmospheric
sources. The major sources of soil lead seem to be paint chips from older houses and deposi-
tion from nearby highways, lead in soil adjacent to a house decreases with distance from the
house; this may be due to paint chips or to dust of atmospheric origin washing from the
rooftop (Wheeler and Rolfe, 1979).
Andresen et al. (1980) reported lead in the litter layer of 51 forest soils in the north-
eastern United States. They found values from 20 to 700 pg/g, which can be compared only
qualitatively to the soil lead concentration cited above. This study clearly shows that the
major pathway of lead to the soil is by the decomposition of plant material containing high
concentrations of atmospheric lead on their surface. Because this organic matter is a part of
the decomposer food chain, and because the organic matter is in dynamic equilibrium with soil
moisture, it is reasonable to assume that lead associated with organic matter is more mobile
than lead tightly bound within the crystalline structure of inorganic rock fragments. This
argument is expressed more precisely in the discussions below.
Finally, a definitive study which describes the source of soil lead was reported by
Gulson et al. (1981) for soils in the vicinity of Adelaide, South Australia. In an urban to
rural transect, stable lead isotopes were measured in the top 10 cm of soils over a 50 km dis-
tance. By their isotopic compositions, three sources of lead were identified: natural, non-
automotive industrial lead from Australia, and tetraethyl lead manufactured in the United
States. The results indicated that most of the soil surface lead originated from leaded gaso-
line. Similar studies have not been conducted in the United States.
PB7/A
7-27
7/14/83
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PRELIMINARY DRAFT
soil in Section 6.5.1. The uptake of lead by plants and its subsequent effect on animals may
be found in Section 8.2. The purpose of this section is to discuss the distribution of lead
in U.S. soils and the impact of this lead on potential human exposures.
7.2.2.1. Typical Concentrations of Lead in Soil.
7.2.2.1.1 Lead in urban, smelter, and rural soils. Shacklette et al. (1971) sampled soils at
a depth of 20 cm to determine the elemental composition of soil materials derived from the
earth's crust, not the atmosphere. The range of values probably represent natural levels of
lead in soil, although there may have been some contamination with anthropogenic lead during
collection and handling. Lead concentrations in soil ranged from less than 10 to greater than
70 pg/g. The arithmetic mean of 20 and geometric mean of 16 ng/fl reflect the fact that most
of the 863 samples were below 30 jjg/g at this depth. McKeague and Wolynetz (1980) found the
same arithmetic mean (20 Mg/fl) for 53 uncultivated Canadian soils. The range was 5 to 50 (jfl/g
and there was no differences with depth between the A, B and C horizons in the soil profile.
Studies discussed in Section 6.5.1 have determined that atmospheric lead is retained in
the upper two centimeters of undisturbed soil, especially soils with at least 5 percent
organic matter and a pH of 5 or above. There has been no general survey of this upper 2 cm of
the soil surface in the United States, but several studies of lead in soil near roadsides and
smelters and a few studies of lead in soil near old houses with lead-based paint can provide
the backgound information for determining potential human exposures to lead from soil.
Because lead is immobilized by the organic component of soil (Section 6.5.1), the concen-
tration of anthropogenic lead in the upper 2 cm is determined by the flux of atmospheric lead
to the soil surface. Near roadsides, this flux is largely by dry deposition and the rate de-
pends on particle size and concentration. These factors vary with traffic density and average
vehicle speed (see Section 6.4,1). In general, deposition flux drops off abruptly with
increasing distance from the roadway. This effect is demonstrated in studies which show that
surface soil lead decreases exponentially up to 25 m from the edge of the road. The original
work of Quarles et al. (1974) showed decreases in soil lead from 550 to 40 pg/g within 25 m
alongside a highway with 12,500 vehicles/day in Virginia. Their findings were confirmed by
Wheeler and Rolfe (1979), who observed an exponential decrease linearly correlated with traf-
fic volume. Agrawal et al (1981) found similar correlations between traffic density and road-
side proximity in Baroda City, as did Garcia-Miragaya et al. (1981) in Venzuela and Wong and
Tam (1978) in Hong Kong. The extensive study of Little and Wiffen (1978) is discussed in
Chapter 6. These authors found additional relationships between particle size and roadside
proximity and decreases with depth in the soil profile. The general conclusion from these
studies is that roadside soils may contain atmospheric lead from 30 to 2000 pg/g in excess of
natural levels within 25 meters of the roadbed, all of which is in the upper layer of the soil
PB7/A
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PRELIMINARY DRAFT
off by rain nor taken up through the leaf surface. For many years, plant surfaces have been
used as indicators of lead pollution (Garty and Fuchs, 1982; Pilegaard, 1978; Ratcliffe, 1975;
Ruhling and Tyler, 1969; Tanaka and Ichikuni, 1982). These studies all show that lead on the
surface of leaves and bark is proportional to traffic density and distance from the highway,
or more specifically, to air lead concentrations and particle size distributions. Other
factors such as surface roughness, wind direction and speed are discussed in Chapter 6. The
data also show that lead in internal plant tissues is directly related to lead in soil.
In a study to determine the background concentrations of lead and other metals in agri-
cultural crops, the Food and Drug Administration (Wolnik et al., 1983), in cooperation with
the U.S. Department of Agriculture and the U.S. Environmental Protection Agency, analyzed over
1500 samples of the most common crops taken from a cross section of geographic locations.
Collection sites were remote from mobile or stationary sources of lead. Soil lead concentra-
tions were within the normal range (8-25 mq/q) of U.S. soils. Extreme care was taken to avoid
contamination during collection, transportation, and analysis. The concentrations of lead in
crops found by Wolnik et al. (1983) are shown as "Total" concentrations in Table 7-9. The
breakdown by source of lead is discussed below. The total concentration data should probably
be seen as representing the lowest concentrations of lead in food available to Americans. It
is likely that lead concentrations in crops harvested by farmers are somewhat higher for
several reasons: some crops are grown closer to highways and stationary sources of lead than
those sampled by Wolnik et al. (1983); some harvest techniques used by farmers might add more
lead to the crop than did Wolnik et al.; and some crops are grown on soils significantly
higher in lead than those of the Wolnik et al. study because of a history of fertilizer ad-
ditions or sludge applications.
Because the values reported by Wolnik et al. are of better quality than previously
reported data for food crops, it is necessary to disregard many other reports as being either
atypical or erroneous. Studies that specifically apply to roadside or stationary source con-
ditions, however, may be applicable if the data are placed in the context of these recent
findings by Wolnik et al. (1983). Studies of the lead associated with crops near highways
have shown that both lead taken up from soil and aerosol lead delivered by deposition are
found with the edible portions of common vegetable crops. However, there is enormous vari-
ability in the amount of lead associated with such crops and in the relative amounts of lead
1n the plants versus on the plants. The variability depends upon several factors, the most
prominent of which are the plant species, the traffic density, the meteorological conditions,
and the local soil conditions (Welch and Dick, 1975; Rabinowitz, 1974; Arvik, 1973; Dedolph et
PB7/A
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PRELIMINARY DRAFT
7.2.2.1.2 Natural and anthropogenic sources of soil lead. Although no study has clearly
identified the relative concentrations of natural and anthropogenic lead in soil, a few clari-
fying statements can be made with some certainty. Lead may be found in inorganic primary
minerals, on humic substances, complexed with Fe-Mn oxide films, on secondary minerals or in
soil moisture. All of the lead in primary minerals is natural and is bound tightly within the
crystalline structure of the minerals. Most of this lead can be released only by harsh treat-
ment with acids. The lead on the surface of these minerals is leached slowly into the soil
moisture. Atmospheric lead forms complexes with humic substances or on oxide films that are
In equilibrium with soil moisture, although the equilibrium strongly favors the complexing
agents. Consequently, the ratio of anthropogenic to natural lead in soil moisture depends
mostly on the amounts of each type of lead in the complexing agents and very little on the
concentration of natural lead in the inorganic minerals.
Except near roadsides and smelters, only a few pg of atmospheric lead have been added to
each gram of soil. Several studies indicate that this lead is available to plants (Section
8.3.1.1) and that even with small amounts of atmospheric lead, about 75 percent of the lead in
soil moisture is of atmospheric origin. A conservative estimate of 50 percent is used in the
discussions in Section 7.3.1.2. A breakdown of the types of lead in soil may be found in
Table 7-8.
TABLE 7-8. SUMMARY OF SOIL LEAD CONCENTRATIONS?
Natural
Atmospheric
Total
lead
lead
lead
Matrix
Rural
Urban
Rural
Urban
Total soil
8-25
3
50-150
10-30
150-300
Primary minerals
8-25
-
-
8-25
8-25
Humic substances*
20
60
2000
80
2000
Soil moisture
0.0005
0.0005
0.0150
0.001
0.0155
t All values in pg/g-
*Assumes 5% organic matter, pH 5.0; may also include lead in Fe-Mn oxide films.
Source: Section 6.5.1
7.2.2.2 Pathways of Soil Lead to Human Consumption.
7.2.2.2.1 Crops. Lead on the surfaces of vegetation may be of atmospheric origin, or a com-
bination of atmospheric and soil in the internal tissues. As with soils, lead on vegetation
surfaces decreases exponentially with distance away from roadsides and smelters (Cannon and
Bowles, 1962; see also Chapter 8). This deposited lead is, persistent. It is neither washed
PB7/A
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PRELIMINARY DRAFT
of the same types of crops taken from actual agricultural situations by Wolnik et al. (1983).
Dedolph et al. (1970) found that while ryegrass and radish leaves grown near a busy highway
contained deposited airborne lead, the fedible portion of the radish was unaffected by varia-
tions in either soil lead or air lead.
To estimate the distribution of natural and atmospheric lead in food crops (Table 7-9),
it is necessary to recognize that some crops of the Wolnik et al. study have no lead from
direct atmospheric deposition, that all lead comes through soil moisture. The lowest concen-
trations of lead are found in those crops where the edible portion grows above ground and is
protected from atmospheric deposition (sweet corn and tomatoes). Belowground crops are also
protected from atmospheric deposition but have slightly higher concentrations of lead, partly
because lead accumulates in the roots of plants (potatoes, onions, carrots). Leafy above-
ground plants (lettuce, spinach, wheat) have even higher lead concentrations presumably
because of exposure to atmospheric lead. The assumption that can be made here is that, in the
absence of atmospheric deposition, exposed aboveground plant parts would have lead concentra-
tions similar to protected aboveground parts.
The data on these ten crops suggest that root vegetables have lead concentrations between
0.0046 and 0.009 pg/g, all soil lead, which presumably is half natural and half anthropogenic
(called indirect atmospheric lead here). Aboveground parts not exposed to significant amounts
of atmospheric deposition (sweet corn and tomatoes) have less lead Internally, also equally
divided between natural and indirect atmospheric lead. If it is assumed that this same con-
centration is the internal concentration for aboveground parts for other plants, it is ap-
parent that five crops have direct atmospheric deposition in proportion to surface area and
estimated duration of exposure. The deposition rate of 0.04 ng/cm2-day in rural environments
(see Section 6.4.1) could account for these amounts of direct atmospheric lead.
In this scheme, soybeans and peanuts are anomalously high. Peanuts grow underground in a
shell and should be of a lead concentration similar to potatoes or carrots, although peanuts
technically grow from the stem of a plant. Soybeans grow inside a sheath and should have an
internal lead concentration similar to corn. The fact that both soybeans and peanuts are
legumes may Indicate species differences.
The accumulation of lead 1n edible crops was measured by Ter Haar (1970), who showed that
edible plant parts not exposed to air (potatoes, corn, carrots, etc.) do not accumulate atmo-
spheric lead, while leafy vegetables do. Inedible parts, such as corn husks, wheat and oat
chaff, and soybean hulls were also contaminated. These results were confirmed by McLean and
.. • win* . i i
Shields (1977), who found that most of the lead in food crops is on leaves and husks. The
general conclusion from these studies is that lead in food crops varies according to exposure
to the atmosphere and in proportion to the effort taken to separate husks, chaff, and hulls
from edible parts during processing for human or animal consumption.
PB7/A 7-31 7/14/83
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PRELIMINARY DRAFT
These discussions lead to the conclusion that root parts and protected aboveground parts
of edible crops contain natural lead and indirect atmospheric lead, both derived from the
soil. For exposed aboveground parts, any lead in excess of the average found on unexposed
aboveground parts is considered to be the result of direct atmospheric deposition.
Near smelters, Merry et al. (1981) found a pattern different from roadside studies cited
above. They observed that wheat crops contained lead in proportion to the amount of soil
lead, not vegetation surface contamination. A similar effect was reported by Harris (1981).
7.2.2.2.2 Livestock. Lead in forage was found to exceed 950 yg/g within 25 m of roadsides
with 15,000 or more vehicles per day (Graham and Kalman, 1974. At lesser traffic densities,
200 jjg/g were found. Other reports have observed 20 to 660 pg/g with the same relationship to
traffic density and distance from the road (see review by Graham and Kalman, 1974). A more
recent study by Crump and Barlow (1982) showed that the accumulation of lead in forage is di-
rectly related to the deposition rate, which varied seasonally according to traffic density.
The deposition rate was measured using the moss bag technique, in which bags of moss are
exposed and analyzed as relative indicators of deposition flux. Rain was not effective in
removing lead from the surface of the moss.
7.2.3 Lead in Surface and Ground Water
Lead occurs in untreated water in either dissolved or particulate form. Dissolved lead is
operationally defined as that which passes through a 0.45 pm membrane filter. Because atmos-
pheric lead in rain or snow is retained by soil, there is little correlation between lead in
precipitation and lead in streams which drain terrestrial watersheds. Rather, the important
factors seem to be the chemistry of the stream (pH and hardness) and the volume of the stream
flow. For groundwater, chemistry is also important, as is the geochemical composition of the
water-bearing bedrock.
Of the year-round housing units in the United States, 84 percent receive their drinking
water from a municipal or private supply of chemically treated surface or ground water. The
second largest source is privately owned wells (Bureau of the Census, 1982). In some communi-
ties, the purchase of untreated bottled drinking water is a common practice. The initial con-
centration of lead in this water, depends largely on the source of the untreated water.
7.2.3.1. Typical Concentrations of Lead in Untreated Water.
7.2.3.1.1 Surface water. Durum et al. (1971) reported a range of 1 to 55 pg/1 in 749 surface
water samples in the United States. Very few samples were above 50 pg/1, and the average was
3.9 mq/1 ¦ Chow (1978) reviewed other reports with mean values between 3 and 4 pg/1. The
National Academy of Sciences (1980) reported a mean of 4 pg/1 with a range from below
detection to 890 \tg/1. Concentrations of 100 Mfl/1 wee found near sites of sewage treatment,
urban runoff, and industrial waste disposal.
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PRELIMINARY DRAFT
Because 1 pg/1 was at or below the detection limit of most investigators during the
1970's, it is likely that the mean of 3 to 4 pg/1 was unduly influenced by a large number of
erroneously high values at the lower range of detection. On the other hand, Patterson (1980)
reports values of 0.006 to 0.05 pg/1 for samples taken from remote streams. Extreme care was
taken to avoid contamination and analytical techniques sensitive to less than 0.001 pg/1 were
used.
Streams and lakes are influenced by their water chemistry and the lead content of their
sediments. At neutral pH, lead moves from the dissolved to the particulate form and the part-
icles eventually pass to sediments. At low pH, the reverse pathway generally takes place.
Hardness, which is a combination of the Ca and Mg concentration, also can influence lead con-
centrations. At higher concentrations of Ca and Mg, the solubility of lead decreases.
Further discussion of the chemistry of lead in water may be found in Sections 6.5.2.1 and
8.2.2.
7.2.3.1.2 Ground water. Municipal and private wells account for a large percentage of the
drinking water supply. This water typically has a neutral pH and somewhat higher hardness
than surface water. Lead concentrations are not influenced by acid rain, surface runoff, or
atmospheric deposition. Rather, the primary determinant of lead concentration is the geo-
chemical makeup of the bedrock that is the source of the water supply. Ground water typically
ranges from 1 to 100 pg Pb/1 (National Academy of Sciences, 1980). Again, the lower part of
the range may be erroneously high due to difficulties of analysis. It is also possible that
the careless application of fertilizers or sewage sludge to agricultural lands can cause con-
tamination of ground water supplies.
7.2.3.1.3 Natural vs. anthropogenic lead in water. Although Chow (1978) reports that the na-
tural lead concentration of surface water is 0.5 pg/1, this value may be excessively high. In
a discussion of mass balance considerations (National Academy of Sciences, 1980), natural lead
was suggested to range from 0.005 to 10 pg/l- Patterson (1980) used further arguments to
establish an upper limit of 0.02 \iq/"\ for natural lead in surface water. This upper limit
will be used in further discussions of natural lead in drinking water.
Because ground water is free of atmospheric lead, lead in ground water should probably be
considered natural in origin as it occurs at the well head, unless there is evidence of
surface contamination.
7.2.3.2 Human Consumption of Lead in Water. Whether from surface or ground water supplies,
municipal waters undergo extensive chemical treatment prior to release to the distribution
system. There is no direct effort to remove lead from the water supply. However, some treat-
ments, such as flocculation and sedimentation, may inadvertently remove lead along with other
undesirable substances. On the other hand, chemical treatment to soften water increases the
solubility of lead and enhances the possibility that lead will be added to water as it passes
through the distribution system.
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7.2.3.2.1 Contributions to drinking water. For samples taken at the household tap, lead con-
centrations are usually higher in the initial volume (first daily flush) than after the tap
has been running for some time. Water standing in the pipes for several hours is intermediate
between these two concentrations (Sharrett et al., 1982; Worth et al., 1981). Common plumbing
materials are galvanized and copper pipe; lead solder is usually used to seal the joints of
copper pipes. Lead pipes are seldom in service in the United States, except in the New
England states (Worth et al., 1981).
Average lead content of running water at the household tap is generally lower (8 Mfl/l)
than in some untreated water sources (25 to 30 ng/1) (Sharrett et al., 1982). This implies
either that treatment can remove a portion of the lead or that measurements of untreated water
are erroneously high. If first flush or standing water is sampled, the lead content may be
considerably higher. Sharrett et al. (1982) showed that in both copper and galvanized pipes,
lead concentrations were increased by a factor of two when the sample was taken without first
flushing the line (see Section 7.3.1.3).
The age of the plumbing is an important factor. New copper pipes with lead solder ex-
posed on the inner surface of the joints produce the highest amount of lead in standing water.
After six years, this lead is leached away and copper pipes subsequently have less lead in
standing water than galvanized pipes. Because lead pipes are rarely used in the United
States, exposure from this source will be treated as a special case in Section 7.3.2.1. The
pH of the water is also important; the acid water of some eastern United States localities can
increase the leaching rate of lead from lead pipes or lead solder joints and prevent the
buildup of a protective coating of calcium carbonate plaque.
Table 7-10 summarizes the contribution of atmospheric lead to drinking water. In this
determination, the maximum reported value for natural lead (0.02 pg/1) was used, all ad-
ditional lead in untreated water is considered to be of atmospheric origin, and it is assumed
that treatment removes 85 percent of the original lead, and that any lead added during distri-
bution is non-atmospheric anthropogenic lead.
7.2.3.2.2 Contributions to food. The use of treated water 1n the preparation of food can be
a significant source of lead in the human diet. There, are many uncertainties in determining
this contribution, however. Water used in food processing may be from a municipal supply or a
private well. This water may be used to merely wash the food, as with fruits and vegetables,
or as an actual ingredient. Water lead may remain on food that is partially or entirely de-
hydrated during processing (e.g., pasta). Water used for packing or canning may be used with
the meal or drained prior to preparation. It is apparent from discussions in Section 7.3.1.3
that, considering both drinking water and food preparation, a significant amount of lead can
be consumed by humans from treated water. Only a small fraction of this lead is of atmo-
spheric origin, however.
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PRELIMINARY DRAFT
TABLE 7-10. SUMMARY OF LEAD IN DRINKING WATER SUPPLIES*
Natural
Pb
Indirect
atmospheric
Pb
Direct
atmospheric
Pb
Non-atmospheric
anthropogenic
Pb
Total
Pb
Untreated
Lakes
0.02
15
10
—
25
Rivers
0.02
15
15
—
30
Streams
0.02
2.5
2.5
—
5
Groundwater
3
--
--
--
3
Treated
Surface
0.003
2.5
1.5
4
8
Ground
0.45
••
7.5
8
*units are pg/1.
7.2.4 Summary of Environmental Concentrations of Lead
Lead concentrations in environmental media that are in the pathway to human consumption
are summarized on Table 7-11. These values are estimates derived from the preceding discus-
sions. In each category, a single value is given, rather than a range, in order to facilitate
further estimates of actual human consumption. This use of a single value is not meant to
imply a high decree of certainty in its determination or homogeneity within the human popula-
tion. The units for water are converted from pg/1 as in Table 7-10 to pg/g to facilitate the
discussions of dietary consumption of water and beverages.
TABLE 7-11. SUMMARY OF ENVIRONMENTAL CONCENTRATIONS OF LEAD
Natural
Atmospheric
Total
Medi urn
Pb
Pb
Pb
Air urban (pg/ms)
0.00005
0.8
0.8
rural (pg/m3)
0.00005
0.2
0.2
Soil total (pg/g)
8-25
3.0
15.0
Food crops (pg/g)
0.0025
0.027
0.03
Surface water (pg/g)*
0.00002
0.005
0.005
Ground water (pg/g)*
0.003
—
0.003
*note change in units from Table 7-12.
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Because concentrations of natural lead are generally three to four orders of magnitude
lower than anthropogenic lead in ambient rural or urban air, all atmospheric contributions of
lead are considered to be of anthropogenic origin. Natural soil lead typically ranges from 10
to 30 but much of this is tightly bound within the crystalline matrix of soil minerals
at normal soil pHs of 4 to 8. Lead in the organic fraction of soil is part natural and part
atmospheric. The fraction derived from fertilizer is considered to be minimal. In undis-
turbed rural and remote soils, the ratio of natural to atmospheric lead is about 1:1, perhaps
as high as 1:3. This ratio persists in soil moisture and in internal plant tissues. Thus,
some of the internal lead in crops is of anthropogenic origin, and some is natural. Informa-
tion on the effect of fertilizer on this ratio is not available. Lead 1n untreated surface
water is 99 percent anthropogenic, presumably atmospheric except near municipal waste out-
falls. It is possible that 75 percent of this lead is removed during treatment. Lead in un-
treated ground water is probably all natural.
In tracking air lead through pathways to human exposure, it is necessary to distinguish
between lead of atmospheric origin that has passed through the soil (indirect atmospheric
lead), and atmospheric lead that has deposited directly on crops or water. Because indirect
atmospheric lead will remain in the soil for many decades, this source is insensitive to pro-
jected changes in atmospheric lead concentrations. Regulation of ambient air lead concentra-
tions will not affect indirect atmospheric lead concentrations over the next several decades.
The method of calculating the relative contribution of atmospheric lead to total poten-
tial human exposure relies heavily on the relationship between air concentration and deposi-
tion flux described on Section 6.4. Estimates of contributions from other sources are usually
based on the observed value for total lead concentration from which the estimated contribution
of atmospheric lead is subtracted. Except for the contribution of lead solder in food cans
and paint pigments in dust, there is little or no direct evidence for the contribution of non-
atmospheric anthropogenic lead to the total lead consumption of humans.
7.3 POTENTIAL PATHWAYS TO HUMAN EXPOSURE
The preceding section discussed ambient concentrations of lead in the environment, focus-
ing on levels in the air, soil, food crops, and water. In this section, environmental lead
concentrations are examined from the perspective of pathways to human exposure (Figure 7-1).
Initially, a current baseline exposure scenario is described for an individual with a minimum
amount of daily lead consumption. This person would live and work in a nonurban environment,
eat a normal diet of food taken from a typical grocery shelf, and would have no habits or ac-
tivities that would tend to increase lead exposure, lead exposure at the baseline level 1s
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PRELIMINARY DRAfT
considered unavoidable without further reductions of lead in the atmosphere or in canned
foods. Host of the baseline lead is of anthropogenic origin, although a portion is natural,
as discussed in Section 7. 3.1. 5.
7.3.1 Baseline Human Exposure
To arrive at a minimum or baseline exposure for humans, it is necessary to begin with the
environmental components, air, soil, food crops, and water, which are the major sources of
lead consumed by humans (Table 7-11). These components are measured frequently, even
monitored routinely in the case of air, so that many data are available on.their concentra-
tions. But there are several factors which modify these components prior to actual human ex-
posure. We do not breathe air as monitored at an atmospheric sampling station, we may be
closer to or farther from the source of lead than is the monitor. We may be inside a
building, with or without filtered air; the water we drink does not come directly from a
stream or river. It has passed through a chemical treatment plant and a distribution system.
A similar type of processing has modified the lead levels present In our food.
Besides the atmospheric lead in environmental components, there are two other sources
that contribute to this baseline of human exposure: paint pigments and lead solder (Figure
7-6). Solder contributes directly to the human diet through canned food and copper water dis-
tribution systems. Chips of paint pigments are discussed later under special environments.
But paint and solder are also a source of lead-bearing dusts. The most common dusts in the
baseline human environment are street dusts and household dusts. They originate as emissions
from mobile or stationary sources, as the oxidation products of surface exposure, or as pro-
ducts of frictional grinding processes. Ousts are different from soil in that soil derives
from crustal rock and typically has a lead concentration of 10 to 30 Mfl/fl. whereas dusts come
from both natural and anthropogenic sources and vary from 1,000 to 10,000 n9/9-
The discussion of the baseline human exposure traces the sequence from ambient air to in-
haled air, from soil to prepared food, from natural water to drinking water, and from paint,
solder and aerosol particles to dusts. At the end of this section, Table 7-24 summarizes the
four sources by natural and anthropogenic contributions, with the atmospheric contribution to
the anthropogenic fraction identified. Reference to this table will guide the discussion of
human exposure in a logical sequence that ultimately presents an estimate of the exposure of
the human population to atmospheric lead. To construct this table, it was necessary to make
decisions based on sound scientific judgment, occasionally in the absence of conclusive data.
This method provides a working approach to identifying sources of lead that can be easily
modified as more accurate data become available.
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~0
m
~~i
3>
AUTO
EMISSIONS
INDUSTRIAL
EMISSIONS
CRUSTAL
WEATHERING
AMBIENT
AIR
SOIL
SURFACE AND
GROUND WATER
-4
t
PLANTS
PAINT
PIGMENTS
-er
50
INHALED
DUSTS
FOOD
DRINKING
AIR
WATER
00
U1
,oW#f*">««*>«¦»*****Of patantial laad upoaurawNoharanotot
atmoapharic origin. Soidar is common mn in baiatina axpoauraa and imv raoraaant SO tn 4B m.r..ii A« «f.
baialjna human consumption. Paint pigmants ara ancountarad in oMar housa* and in tofe actfaoant to otdar
-------
PRELIMINARY DRAFT
7.3.1.1 Lead in inhaled Air. A principal determinant of atmospheric lead 1f distance from
the source. At more than 100 m from a major highway or more than 2 km from a stationary
source, lead concentrations generally drop to constant levels (see Section 6.3), and the par-
ticle size distribution shifts from a bimodal distribution to a unlmodal one with a mass
median equivalent diameter of about 0.2 p". Because the concentration of atmospheric lead at
nonurban stations is generally from 0.05 to 0.15 (jg/m3, a value of 0.1 yg/m* may reasonably be
assumed. A correction can be made for the Indoor/outdoor ratio assuming the average Individ-
ual spends 20-22 hours/day 1n an unflltered Inside atmosphere and the average indoor/outdoor
ratio for a nonurban location 1s 0.5 (Table 7-7). The adjusted air concentration becoms 0.05
MSI/in8 for baseline purposes.
The concentration of natural lead in the atmosphere, discussed in Section 7.2.1.1.3, is
probably about 0.00005 pg/ms. This 1s an insignificant amount compared to the anthropogenic
contribution of 0.2 pg/ii8. A summary of lead in inhaled air appears in Table 7-12.
TABLE 7-12. SUMMARY OF INHALED AIR LEAD EXPOSURE
Adjusted
Total
Natural
Direct
air Pb
Amount
lead
Pb
atmospheric
conc.1
inhaled
exposure
(pg/day)
Pb
MQ/m3
(ma/day)
(pg/day)
(pg/day)
Children (2 year-old)
0.05
10
0.5
0.001
0.5
Adult-working inside
0.05
20
1.0
0.002
1.0
Adult-working outside
0.10
20
2.0
0.004
2.0
1Values adjusted for Indoor/outdoor ratio of lead concentrations and for dally time spent
outdoors.
7.3.1.2 Lead 1n Food. The route by which many people receive the largest portion of their
I
daily lead Intake is through foods. Several studies have reported average dietary lead inakes
in the range 100 to 500 pg/day for adults, with individual diets covering a much greater range
(Schroeder and Tipton, 1968; Tepper, 1971; Mahaffey, 1978; Nutrition Foundation, Inc. 1982).
Gross (1981) analyzed results of the extensive lead mass balance experiments described by
Kehoe (1961), which were conducted from 1937 to 1972. According to these data, total dietary
lead intake decreased from approximately 300 pg/day in 1937 to 100 pg/day in 1970, although
there is considerable variability in the data. Only a fraction of this lead 1s absorbed, as
discussed in Chapter 10.
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The amount of lead typically found in plants and animals is discussed in Section 7.2.2.2.
The sources of this lead are air, soil, and untreated waters (figure 7-1). Food crops and
livestock contain lead in varying proportions from the atmosphere and natural sources. From
the farm to the dinner table, lead is added to food as it is harvested, transported, pro-
cessed, packaged, and prepared. The sources of this lead are dusts of atmospheric and indus-
trial origin, metals used in grinding, crushing, and sieving, solder used in packaging, and
water used in cooking.
The American diet is extremely complex and variable among individuals. Pennington (1983)
has described the basic diets, suppressing individual variation but identifying 234 typical
food categories, for Americans grouped into eight age/sex groups (Table 7-13). These basic
diets are the foundation for the Food and Drug Administration's revised Total Diet Study,
often called the market basket study, beginning in April, 1982. The diets used for this dis-
cussion include food, beverages and drinking water for a 2-year-old child, the adult female 25
to 30 years of age and the adult male 25 to 30 years of age. The 234 typical foods that com-
prise the basic diets approximate 90 percent or more of the food actually consumed by partici-
pants in the two surveys which formed the basis of the Pennington study. These 234 categories
have been further reduced to 26 food categories (Table 7-13) and 6 beverage categories (Table
7-20) based on known or presumed similarities in lead concentration, and a weighted average
lead concentration has been assigned to each category from available literature data. A com-
plete list of the Pennington categories and the rationale for grouping into the categories of
Tables 7-13 and 7-20 appears in Tables 7D-1 and 7D-2 of Appendix 70.
Milk and foods are treated separately from water and other beverages because the pathways
by which lead enters these dietary components are substantially different (Figure 7-1), as
solder and atmospheric lead contribute significantly to each. Data for lead concentrations on
Tables 7-13 and 7-20 came from a preliminary report of the 1982 Total Diet Study provided by
the U.S. Food and Drug Administration (1983) for the purpose of this document. In 1982, the
Nutrition Foundation published an exhaustive study of lead in foods, using some data from the
National Food Processors Assocation and some data from Canadian studies by Kirkpatrick et al.
(1980) and Kirkpatrick and Coffin (1974, 1977). A summary of the available data for the
period 1973 to 1980 was prepared in an internal report to the FDA prepared by Beloian (1980).
Portions of these reports were used to interpret the contributions of lead to food during
processing.
Many of the food categories in Table 7-13 correspond directly to the background crop and
meat data presented in Table 7-9. The following section evaluates the amounts of lead added
during each step of the process from the field to the dinner table. In the best case, re-
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PRELIMINARY DRAFT
liable data exist for the specific situation in question and conclusions are drawn. In some
cases, comparable data can be used with a few reasonable assumptions to formulate acceptable
estimates of lead contributions. For a portion of the diet, there are no acceptable data and
the contributions of lead must, for the time, be listed as of undetermined origin.
TABLE 7-13. LEAD CONCENTRATIONS IN MILK AND FOODS
Dietary consumption
(g/day) Lead Summary
Child Adult Adult concentrati on* food
(2-yr-old) female male (Mfl/fl) category
in Table 7-16
Milk
350
190
280
0.01
A
Dairy products
24
36
49
0.03
A
Milk as ingredient
7
11
15
0.01
A
Beef
33
61
120
0.035
B
Pork
12
21
40
0.06
B
Chicken
12
20
29
0.02
B
Fish
5
15
18
0.09
B
Prepared Meats
14
11
23
0.013
B
Other Meats
1
7
5
0.07
B
Eggs
33
34
53
0.017
B
Bread
42
56
75
0.015
C
Flour as ingredient
23
26
79
0.013
C
Non-wheat cereals
33
13
34
0.025
C
Corn flour
14
12
20
0.025
C
Leafy vegetables
7
39
38
0.05
C
Root vegetables
3
7
7
0.025
C
Vine vegetables
19
49
62
0.025
C
Canned vegetables
39
53
62
0.25
0
Sweet corn
4
6
7
0.01
C
Canned sweet corn
5
4
7
0.21
D
Potatoes
38
52
85
0.02
C
Vegetable oil
5
12
15
0.03
c
Sugar
15
21
34
0.03
c
Canned fruits
14
11
13
0.22
0
Fresh fruits
49
57
49
0.02
c
Pureed baby food
11
—•
—
0.03
Subtotal
812
824
1219
Water and
beverages
647
1286
1804
See Table 7-21
Total 1459
2110
5023
"Data are summarized from preliminary data provided by the U.S. FDA; complete data appear in
Appendix 7D.
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7.3.1.2.1 Lead added during handling and transportation to processor. Between the field and
the food processor, lead is added to the food crops. It is assumed that this lead is all of
direct atmospheric origin. Direct atmospheric lead can be lead deposited directly on food
materials by dry deposition, or it can be lead on dust which has collected on other surface*,
then transferred to foods. For the purposes of this discussion, it is not necessary to dis-
tinguish between these two forms, as both are a function of air concentration.
There are no clear data on how much lead is added during transportation, but some obser-
vations are worth noting. First, some fresh vegetables (e.g., potatoes, lettuce, carrots,
onions) undergo no further processing other than trimming, washing and packaging. If washed,
water without soap is used; no additives or preservatives are used. An estimate of the amount
of atmospheric lead added during handling and transportation of all food crops can be made
from the observed increases in lead on those fresh vegetables where handling and transpor-
tation would be the only source of added lead. Because atmospheric lead deposition 1s a
function of time, air concentration, and exposed surface area, there is an upper limit to the
maximum amount of direct atmospheric lead that can be added, except by the accumulation of
atmospheric dusts.
7.3.1.2.2 Lead added during preparation for packaging. For some of the food items, data are
available on lead concentrations just prior to the filling of cans. In the case whare the
food product has not undergone extensive modification (e.g., cooking, added ingredients), the
added lead was most likely derived from the atmosphere or from the machinery used to handle
the product. As with transportation, the addition of atmospheric lead is limited to reason"
able amounts that can be added during exposure to air, and reasonable amounts of atmospheric
dust accumulation on food processing surfaces. One process that may increase the exposure of
the food to air is the use of air 1n separating food items, as in wheat grains from chaff.
Where modification of the food product has occurred, the most common ingredients added
are sugar, salt, and water. It is reasonable that water has a lead concentration similar to
drinking water reported in Section 7.3.1.3 (0.008 Mfl/g) and that sugar (Boyer and Johnson,
1982) and salt have lead concentrations of 0.01 pg/g. Grinding, crushing, chopping, and
cooking may add lead from the metallic parts of machinery and from industrial greases. A
summary of the data (Table 7-14) indicates that about 30 percent of the total lead 1n canned
goods is the result of prepacking processes.
7.3.1.2.3 Lead added during packaging. From the time a product is packaged in bottles, cans
.or plastic containers, until 1t is opened in the kitchen, it may be assumed that no food Item
receives atmospheric-lead.pt Most of the lead which Is added during this stage comes from the
solder used to seal some types of cans. Estimates by the U.S. FDA, prepared in cooperation
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PREUHIIMSy DRAFT
with the National Food Processors Association, suggest that lead in solder contributes more
than 66 percent of the lead in canned foods where • lead solder side sea* was used. This lead
was thought to represent a contribution of 20 percent to the total lead consumption in foods
(F.R., 1979 August 31),
TABLE 7-14. ADDITION Of LEAD TO FOOD PRODUCTS
In the
After
After
After
Total Pb
Food
field
preparation
packaging
kitchen
added
for packaging
preparation
after harvest
Soft Packaged
Wheat
0.037
0.065
—
—
Field corn
0.022
0.14
0.025
0.003
Potatoes
0.009
0.018
0.02
0.011
Lettuce
0.013
0.07
0.015
0.002
Rice
0.007
0.10
0.084
0.077
Carrots
0.009
0.05
0.017
0.008
ieef
0.01
0.07
0.03S
0.025
Pork
0.06
0.10
0.06
--
Sweet com
0.003
0.04
0.27
0.28
0.28
Torntoes
0.002
0.06
0.29
—
Spinach
0.045
0.43
0.68
0.86
0.82
Peas
0.08
0.19
0.22
0.14
Applesauce
0.08
0.24
0.17
0.09
Apricots
0.07
0.17
--
0.10
Nixed fruit
0.08
0.24
0.20
0.12
Plums
0.09
0.16
0.07
Green beans
0.16
0.32
0.16
•-
This table sumarizes the stepwise addition of lead to food products at several stages between
the field and the dinner table. Data are in jjg/g fresh weight.
The full extent of the contribution of the canning process to overall lead level* in
albacor* tuna was reported in a benchmark study by Settle and Patterson (1986). Using rigor-
ous clean laboratory procedures, these investigators analysed lead in fresh tuna, as well as
In tuna packaged fn soldered and unsoldered cans. The data, presented in Table 7-15, show
that lead concentrations in canned tuna are elevated above levels in fresh tuna by a factor of
4,000, and by a factor of 40,MO above natural levels of lead in tuna. Nearly all of the in-
crease results frost leaching of the lead froa the soldered sea»-t*f the can; tuna ftroa an
unsoldered can is elevated by a factor of only 20 compared with tuna fresh from the sea. Note
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PRELIMINARY DRAFT
that when fresh tuna 1s dried and pulverized, as in the National Bureau of Standards reference
material, lead levels are seen to increase by a factor of 400 over fresh sea tuna. Table 7-15
also shows the results of analyses conducted by the National Marine Fisheries Service.
TABLE 7-15. PREHISTORIC AND MODERN CONCENTRATIONS IN HUMAN FOOD
FROM A MARINE FOOD CHAIN1
Estimated
prehistoric
Modern
Surface seawater
0.0005
0.005
Albacore muscle, fresh
0.03
0.3
Albacore muscle from die-punched
unsoldered can
—
7.0
Albacore muscle, lead-soldered can
—
1400
Anchovy from albacore stomach
2.1
21
Anchovy from lead-soldered can
--
4200
'Values are ng/g fresh weight.
Source: Settle and Patterson (1980).
7.3.1.2.4 Lead added during kitchen preparation and storage. Although there have been
several studies of the lead concentrations in food after typical meal preparation, most of the
data are not amenable to this analysis. As a part of its compliance program, the U.S. FDA has
conducted the Total Diet Study of lead and other trace contaminants in kitchen-prepared food
each year since 1973. Because the kitchen-prepared items were composited by category, there
1s no direct link between a specific food crop and the dinner table. Since April, 1982, this
survey has analyzed each food item individually (Pennington, 1983).
Other studies which reflect contributions of lead added during kitchen preparation have
been conducted. Capar (1978) showed that lead in acidic foods that are stored refrigerated in
open cans can increase by a factor of 2 to 8 in five days if the cans have a lead-soldered
side seam not protected > by an interior lacquer coating. Comparable products in cans with the
lacquer coating or in glass jars showed little or no increase.
PB7/A
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7.3.1.2.5 Recent changes of lead in food. As a part of its program to reduce the total lead
intake by children (0 to 5 years) to less than 100 Mg/day by 1988, the U.S. FDA estimated lead
intakes for individual children in a large-scale food consumption survey (Beloian and
McDowell, 1981). To convert the survey of total food intakes into lead intake, 23 separate
government and industry studies, covering the period from 1973 to 1978, were statistically
analyzed. In spite of the variability that can occur among individuals grouped by age, the
authors estimated a baseline (1973-78) daily lead intake of II Mg/day for infants aged 0 to 5
months, 59 pg/day for children 5 to 23 months, and 82 jjg/day for children 2 to 5 years. Bet-
ween 1973 and 1978, Intensive efforts were made by the food industry to remove sources of lead
from Infant food items. By 1980, there had been a 47 percent reduction in the lead consump-
tion of the age group 0 to 5 months and a 7 percent reduction for the 6 to 23 month age group
(Table 7-16). Most of this reduction was accomplished by the discontinuation of soldered cans
used for infant formula.
TABLE 7-16. RECENT TRENDS OF LEAD CONCENTRATIONS IN FOOD ITEMS
Early 70's
(Mg/g)
1976-77
(Mg/g)
1980-81
(Mg/g)
1982
(pg/g)
Canned food1
Green beans 0.32
Beans w/pork 0.64
Peas 0.43
Tomatoes 0.71
Beets 0,38
Tomato juice 0.34
Applesauce 0.32
Citrus juice 0.14
Infant food2
Formula concentrate 0.10
Juices 0.30
Pureed foods 0.15
Evaporated milk 0.52
data
not
available
0.055
0.045
0.05
0.10
0.32
0.26
0.19
0.29
0.24
0.08
0.04
0.11
0.01
0.015
0.02
0.07
0,16
0.17
0.22
0.12
0.067
0.17
0.04
1Boyer and Johnson (1982); 1982 data from U.S. Food and Drug Administration (1983).
2Pre-1982 data from early 70's and 1976-79 from Jelinek (1982); 1980-81 data from Schaffner
etal. (1983).
The 47 percent reduction in dietary lead achieved for infants prior to 1980 came about
largely because there are relatively few manufacturers of foods for infants and it was compar-
atively simple for this industry to mount a coordinated program in cooperation with the U.S.
PB7/A 7-45 7/14/83
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PRELIMINARY DRAFT
FBA. There has not yet been a similar decrease in adult foods (Table 7-16) because only a few
Manufacturers have switched to non-lead cans. As the switchover increases, lead in canned
food should decrease to a level as low as 30 percent of the pre-1978 values, and there should
be a corresponding decrease of lead in the total adult diet, perhaps as such as 25 to 30 per-
cent. The use of lead-soldered cans in the canning industry has decreased fro* 90 percent in
1979 to 63 percent in 1982. By the end of 1984, the two leading can manufacturers expect to
produce no more lead-soldered cans for the food industry. A two-year time lag is expected
before the last of these cans disappears from the grocery shelf. Some of the 23 saaller
Manufacturers of cans have announced siailar plans over a longer period of tiae. It is likely
that any expected decrease in the contribution of air lead to foods will be complemented by a
decrease in lead from soldered cans.
7.3.1.2.6 Summary of lead in food. The data of Table 7-13 have been condensed to four cate-
gories from the 26 categories of food in Table 7-17. The total lead concentrations are
weighted according to consultion froai Table 7-13, then broken down by source based on the in-
formation provided in Tables 7-9 and 7-14, which show estimates of the atmospheric lead added
before and after harvest. The same weighted total lead concentrations are used to estimate
¦ilk and food lead consumption in Table 7-18 for three age/sex categories. The total dietary
lead consumption is then broken down by source in Table 7-19, using the distributions of Table
7-17. Because the percent distribution by source is approximately the same for the three age/
sex categories, only the data for adult males are shown.
TABLE 7-17. SUMAffY OF LEAD CONCfNTRATIONS IN MILK AND FOODS BY SOURCE*
Pb of %
Major
Direct
Pb from
undeter-
Direct
food
Total
atmospheric
solder &
mined
atmospheric
category
lead
lead
other metals
origin
lead
A. Dairy
0.013
0.007
—
0.007
54%
B. Heat
0.036
0.02
0.02
0.016
sex
C. Food craps
0.022
0.016
—
0.002
m
0. Canned food
0.24
0.016
0.20
0.02
7t
"Foods have been categorized from Table 7-13. Data are in pg/g. The natural and indirect
atmospheric lead concentrations in dairy and meat products are estimated to be 0.0002 w/q
frm each source. In food crops and canned foods, these values are 0.002 pg/g.
PB7/A
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It Is apparent that at least 35 percent of lead in milk Mud foot cm it attrfthtttMl t»
direct atmospheric deposition, compared to 26 percent fro* solder
-------
PRELIMINARY DRAFT
The major source of lead contamination in drinking water is the water supply system it-
self. Water that is corrosive can leach considerable amounts of lead from lead plumbing and
lead compounds used to join pipes. Moore (1977) demonstrated the effect of water standing in
pipes overnight. Lead concentrations dropped significantly with flushing at 10 1/min for five
minutes (Figure 7-7). Lead pipe currently is in use in some parts of New England for water
service lines and Interior plumbing, particularly in older urban areas. The contributions of
lead plumbing to potential human exposure are considered additive rather than baseline and are
discussed in Section 7.3.2.1.3.
There have been several studies in North America and Europe of the sources of lead in
drinking water. A recent study in Seattle, WA by Sharrett et al. (1982) showed that the age
of the house and the type of plumbing determined the lead concentration in tap water. Stand-
ing water in copper pipes from houses newer than five years averaged 31 yg/1; those less than
18 months average about 70 yg/1. Houses older than five years and houses with galvanized pipe
averaged less than 6 yg/1. The source of the water supply, the length of the pipe and the use
of plastic pipes in the service line had little or no effect on the lead concentrations. It
appears certain that the source of lead in new homes with copper pipes is the solder used to
join these pipes, and that this lead is eventually leached away with age.
The Sharrett et al. (1982) study of the Seattle population also provided data on water
and beverage consumption which extended the scope of the Pennington (1983) study of all Ameri-
cans. While the total amount of liquids consumed was slightly higher in Seattle (2200 g/day
vs. 1800 g/day for all Americans), the breakdown between water consumed inside and outside the
home can prove useful. Men, women and children consume 53, 87, and 87 percent respectively of
their water and beverages within the home.
Bailey and Russell (1981) have developed a model for population exposure to lead in home
drinking water. The model incorporates data for lead concentration as a function of stagna-
tion time in the pipes, as well as probability distributions for times of water use throughout
the day. Population surveys conducted as part of the United Kingdom Regional Heart Survey
provided these water-use distributions.
Other studies have been conducted in Canada and Belgium. Lead levels in water boiled in
electric kettles were measured in 574 households in Ottawa (Wigle and Charlebois, 1978). Con-
centrations greater than 50 |jg/l were observed in 42.5 percent of the households, and ex-
cessive lead levels were associated with kettles more than five years old.
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PRELIMINARY DRAFT
TIME OF FLUSHING, mJnutM
Figure 7-7. Change in drinking water iaad concentration in a house with
lead plumbing for the first use of water in the morning. Hushing rate was
10 liters/minute.
Source: Moore <1977).
023PB8/B
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7/01/83
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PRELIMINARY DRAFT
mit 7-if.
HHMf SY SOURCE OF LEAD CONSUMED FROM MILK AND FOODS*
Total
Natural
Atmospheric lead
Pb from
Lead of
lead
lead
solder and
undeter-
Indirect
Direct
other
mined
lead
lead
metals
origin
A. tolry
4.5
0.1
0.1
2.3
2.0
B. Meat
10.4
0.1
0.1
5.7
—
4.5
C, Food crops
11.1
1.0
1.0
8.1
—
1.0
0, Canned foods
19.7
0.2
0.2
1.3
16.4
1.6
Total
45.7
1.4
1.4
17.4
16.4
9.1
* of total
1O05S
3.1%
3.1X
38. IS
35.9X
19.9*
•distribution based on adult male diet. Data are In pg/day. There nay be some direct
atmospheric lead and solder lead in the category of undetermined origin.
The potential exposure to lead through water and beverages is presented in Tables 7-20,
7-21 and 7-22. In Table 7-20, typical concentrations of lead in canned and bottled beverage*
and fn beverages made from tap water (e.g., coffee, tea, drinking water) are shown by source.
The baseline concerrtratfcm of water is taken to be 0.01 vg/g, although 0.006 to 0.008 are
often cited In the literature for specific locations. It is assumed that 2/3 of the original
lead fs lost during water treatment and that only 0.005 mq/q remains from direct atmospheric
deposition. The water distribution system adds 0.001 pg/g, shown here as lead of undetermined
origin. The source appears to be the pipes or the solder used to seal the pipes. These
Values are used for water in canned and bottled beverages, with additional amounts added fro*
•older and other packaging procedures.
The lead concentration* in beverages are multiplied by total consumption to get daily
lead consumption in Table 7-21 for 3 age/sex categories. For adult males, these are
summarized by source of lead in Table 7-22; distribution by source would be proportional for
children and adult females. The data of Table 7-22 are used for the overall summary of base-
line human exposure in Section 7.3.1.5.
7.3.1.4 Uad In Ousts. By technical definition, dusts are solid particles produced by the
disintegration of materials (Friedlander, 1977) and appear to have no size limitations.
Although dusts are of complex origin, they may be placed conveniently into a few categories
relating to human exposure. Generally, the.most convenient categories are household dusts,
soil dust, street dusts and occupational dusts. It is a characteristic of dust particles that
they accumulate on exposed surfaces and are trapped 1n the fibers of clothing and carpets.
Ingestion of dust particles, rather than inhalation, "appears to be the greater problem in the
baseline environment, especially ingestion during meals and playtime activity by small chil-
dren.
mm/t 7-50 7/14/83
-------
TABLE 7-20. SUMMARY BY SOURCE OF LEAD CONCENTRATIONS IN WATER
AND BEVERAGES*
Di rect
Lead fro*
Percent
Total
atmospheric
solder and
direct
lead
lead
other aetals
atmospheric
Canned juices
0.052
0.0015
0.048
2.9%
Frozen juices
0.02
0.0015
0.014
7.5
Canned soda
0.033
0.0015
0.029
4.5
Bottled soda
0.02
0.0015
0.014
7.5
Canned beer
0.017
0.0015
0.013
8.8
Water & beverages
0.008
0.0015
0.004
18.9
*Qata are In pg/g. Natural and indirect atmospheric lead are estisated to be 0.00002 and
0.0025 Mg/g respectively, for all beverage types.
-------
TABLE 7-21. DAILY CONSUMPTION AND POTENTIAL LEAD EXPOSURE FROM
WATER AND BEVERAGES
Consumption* Beverage Lead consumption
(g/day) lead (iio/day)
2 yr old Adult Adult conc.t 2 yr old Adult Adult
Beverage child female nale (pg/g) child female male
Canned juices
53
28
20
0.052
2.8
1.5
1.0
Frozen juices
66
66
73
0.02
1.3
1.3
1.5
Canned soda
75
130
165
0.033
2.5
4.3
5.4
Bottled soda
75
130
165
0.02
1.5
2.6
3.3
Coffee
2
300
380
0.01
-
3.0
3.8
Tea
32
160
140
0.01
0.3
1.6
1.4
Canned beer
-
35
300
0.017
-
0.6
5.1
Wine
-
35
11
0.01
-
0.1
0.1
Whi skey
-
5
9
0.01
.
0.1
0.1
Water
320
400
510
0.008
2.6
2.6
3.2
Water as ingredient
24
20
31
0.008
0.2
0.2
0.2
Total 647 1286 1804 11.2 17.9 25.1
* Data from Pennington, 1983.
f Data froa U.S. Food and Drug Administration, 1983.
-------
PRELIMINARY DRAFT
TABLE 7-22. SUMMARY BY SOURCE OF LEAD CONSUMED IN WATER AND BEVERAGES*
Natural and
Lead in
indirect
Direct
solder and
Total
atmospheric
atmospheric
other metals
Pb
Pb
Pb
Pb
Canned juices
1.0
0.05
0.03
0.92
Frozen juices
1.5
0.18
0.11
1.2
Canned soda
5.4
0.42
0.25
4.7
Bottled soda
3.3
0.50
0.3
2.5
Canned beer
5.1
0.8
0.5
3.8
Water &
beverages
8.8
2.8
1.6
4.4
Total
25.1
4.8
2.8
17.5
Percent
100%
19.1%
11. IX
69.7%
*Data are for adult males, expressed in pg/day. Percentages are the same for children
and adult females. Total consumption for children and adult females shown on Table 7-21.
Two other features of dust are important. First, they must be described in both concen-
tration and amount. The concentration of lead in street dust may be the same in a rural and
urban environment, but the amount of dust may differ by a wide margin. Secondly, each cate-
gory represents some combination of sources. Household dusts contain some atmospheric lead,
some paint lead and some soil lead. Street dusts contain atmospheric, soil, and occasionally
paint lead. This apparent paradox does not prevent the evaluation of exposures to dust, but
it does confound efforts to identify the amounts of atmospheric lead contributed to dusts.
For the baseline human exposure, it is assumed that workers are not exposed to occupational
dusts, nor do they live in houses with interior leaded paints. Street dust, soil dust and
some household dust are the primary sources for baseline potential human exposure.
In considering the impact of street dust on the human environment, the obvious question
arises as to whether lead in street dust varies with traffic density. Nriagu (1978) reviewed
several studies of lead in street dust. The source of lead was probably flue dust from burn-
ing coal. Warren et al. (1971) reported lead in street dust of 20,000 pg/fl in a heavily traf-
ficked area. In the review by Nriagu (1978), street dust lead concentrations ranged from 300
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PRELIMINARY DRAFT
to 18,000 pg/g 1n several cities in the United States. In Hong Kong, lead in street dust
ranged from 960 to 7400 pg/g with no direct relationship to traffic volume (Ho, 1979). In
other reports from Hong Kong, lau and Wong (1982) found values from 130 pg/g at 20 vehicles/
day to 3,900 pg/g at 37,000 vehicles/day. Fourteen sites in this study showed close correla-
tion with traffic density.
In the United Kingdom, lead in urban and rural street dusts was determined to be 970 and
85 pg/g, respectively, by Oay et al, (1975). A later report by this group (Day et al. , 1979)
discusses the persistency of lead dusts in rainwashed areas of the United Kingdom and New
Zealand and the potential health hazard due to ingestion by children. They concluded that,
whereas the acidity of rain was insufficient to dissolve and transport lead particles, the
potential health hazard lies with the ingestion of these particles during the normal play
activities of children residing near these areas. A child playing at a playground near a
roadside might consume 20 to 200 pg lead while eating a single piece of candy with unwashed
hands. It appears that in nonurban environments, lead in street dust ranges from 80 to 130
pg/g, whereas urban street dusts range from 1,000 to 20,000 pg/g. For the purpose of esti-
mating potential human exposure, an average lead value of 90 pg/g in street dust is assumed
for baseline exposure on Table 7-23, and 1500 pg/g in the discussions of urban environments in
Section 7.3.2.1.
Dust is also a normal component of the home environment. It accumulates on all exposed
surfaces, especially furniture, rugs and wlndowsilIs. For reasons of hygiene and respiratory
health, many homemakers take great care to remove this dust from the household. Because there
are at least two circumstances where these measures are inadequate, it is important to
consider the possible concentration of lead in these dusts in order to determine potential ex-
posure to young children. First, some households do not practice regular dust removal, and
secondly, in some households of workers exposed occupationally to lead dusts, the worker may
carry dust home in amounts too small for efficient removal but containing lead concentrations
much higher than normal baseline values.
In Omaha, Nebraska, Angle and Mclntire (1979) found that lead in household dust ranged
from 18 to 5600 pg/g. In Lancaster, England, a region of low industrial lead emissions,
Harrison (1979) found that household dust ranged from 510 to 970 pg/g, with a mean of 720
pg/g. They observed soil particles (10 to 200 pm in diameter), carpet and clothing fibers,
animal and human hairs, food particles, and an occasional chip of paint. The previous Lead
Criteria Oocument (U.S. Environmental Protection Agency, 1977) summarized earlier reports of
lead in household dust showing residential suburban areas ranging from 280 to 1,500 pg/g,
urban residential from 600 to 2,000 pg/g, urban industrial from 900 to 16,000 pg/g. In El
Paso, Texas, lead in household dust ranged from 2,800 to 100,000 pg/g within 2 km of a smelter
(Landrigan et al. 1975).
023PB8/B 7-54 7/14/83
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PRELIMINARY DRAFT
It appears that most of the values for lead in dust 1n nonurban household environments
fall in the range of 50 to 500 yg/g. A mean value of 300 pg/g is assumed. The only natural
lead in dust would be some fraction of that derived from soil lead. A value of 10 pg/g seems
reasonable, since some of the soil lead is of atmospheric origin. Since very little paint
lead is included in the baseline estimate, most of the remaining dust lead would be from the
atmosphere, Table 7-23 summarizes these estimates of human exposure to dusts for children and
adults. It assumes that children ingest about 5 times as much dust as adults, most of the ex-
cess being street dusts from sidewalks and playgrounds. Exposure of children to occupational
lead would be through contaminated clothing brought home by parents. Host of this lead is of
undetermined origin because no data exist on whether the source is dust similar to household
dust or unusual dust from the grinding and milling activities of factories.
7.3.1.5 Summary of Baseline Human Exposure to Lead. The values derived or assumed in the
preceeding sections are summarized on Table 7-24. These values represent only consumption,
not absorption of lead by the human body. The key question of what are the risks to human
health from these baseline exposures is addressed in Chapter 13. The approach used here to
evaluate potential human exposure is similar to that used by the National Academy of Sciences
(1980) and the Nutrition Foundation (1982) in their assessments of the impact of lead in the
human environment.
TABLE 7-23. CURRENT BASELINE ESTIMATES OF POTENTIAL HUMAN EXPOSURE TO DUSTS
Dust Dust
lead Dust lead
conc. ingested consumed Source of lead (uq/day)
pg/g g/day pg/day Natural Atmos. Undetermined
Child
Household dusts
Street dust
Occupational dust
Total
Percent
300
90
150
0.05
0.04
0.01
0.10
15
4.5
1.5
21.0
100%
0.5
0.1
0.6
2.8
14.5
4.5
19.0
90.5
1.4
1.4
6.7
Adult
Household dusts
Street dust
Occupational dust
Total
Percent
300
90
150
0.01
0.01
0.02
3
1.5
4.5
100%
0.1
0.1
0.2
4.5
2.9
2.9
64.4
1.4
1.4
31.1
023PB8/B
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7/14/83
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PRELIMINARY DRAFT
TABLE 7-24. SUttlARY OF BASELINE HUHAN EXPOSURES TO LEADt
Source
Total
lead
consumed
Natural
lead
consumed
Soil
Indirect
atmospheric
lead*
Direct
atmospheric
lead*
Lead from
solder or
other metals
Lead of
undetermined
origin
Chlld-2 yr old
Inhaled air
0.5
0.001
-
0.5
-
-
Food
28.7
0.9
0.9
10.9
10.3
17.6
Water & beverages
11.5
0.01
2.1
1.2
7.8
-
Oust
21.0
0.6
~
19.0
I—
1.4
Total
61.4
1.5
3.0
31.6
18.1
19.0
Percent
100%
2.4%
4.9%
51.5%
29.5%
22.6%
Adult female
Inhaled air
1.0
0.002
-
1.0
-
-
Food
33.2
1.0
1.0
12.6
11.9
21.6
Water & beverages
17.9
0.01
3.4
2.0
12.5
-
Oust
4.5
0.2
*
2.9
1.4
Total
56.6
1.2
4.4
18.5
24.4
23.0
Percent
100%
2.1*
7.8%
32.7%
43.1%
26.8%
Adult male
Inhaled air
1.0
0.002
-
1.0
-
-
Food
45.7
1.4
1.4
17.4
16.4
31.5
Water & beverages
25.1
0.1
4.7
2.8
17.5
-
Oust
4.5
0.2
_2_
2.9
"
1.4
Total
76.3
1.7
6.1
24.1
33.9
32.9
Percent
100%
2.2%
8.0%
31.6%
44.4%
27.1%
'Indirect atmospheric lead has been previously Incorporated Into soil, and will probably remain In the
soil for decades or longer. Direct ataospherlc lead has been deposited on the surfaces of vegetation
+and living areas or Incorporated during food processing shortly before human consumption.
Units are 1n tig/day.
7.3.2 Additive Exposure Factors
There are many conditions, even in nonurban environments, where an individual may
increase his lead exposure by choice, habit, or unavoidable circumstance. The following sec-
tions describe these conditions as separate exposures to be added as appropriate to the base-
line of human exposure described above. Most of these additive exposure clearly derive from
air or dust, while few derive from water or food.
7.3.2.1 Living and Working Environments With Increased Lead Exposure. Ambient air lead con-
centrations are typically higher in an urban than a rural environment. This factor alone can
contribute significantly to the potential lead exposure of Americans, through increases in
023PB8/B
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PRELIMINARY DRAFT
inhaled air and consumed dust. Produce from urban gardens may also increase the daily con-
sumption of lead. Some environmental exposures may not be related only to urban living, such
as houses with interior lead paint or lead plumbing, residences near smelters or refineries,
or family gardens grown on high-lead soils. Occupational exposures may also occur in an urban
or rural setting. These exposures, whether primarily in the occupational environment or
secondarily in the home of the worker, would be additive with other exposures in an urban
location or with special cases of lead-based paint or plumbing.
7.3.2.1.1 Urban atmospheres. Urban atmospheres have more airborne lead than do nonurban
atmospheres, therefore there are increased amounts of lead in urban household and street dust.
Typical urban atmospheres contain 0.5 to 1.0 pg Pb/m3. Other variables are the amount of in-
door filtered air breathed by urban residents, the amount of time spent indoors, and the
amount of time spent on freeways. Dusts vary from 500 to 3000 pg Pb/g in urban environments.
It 1s not known whether there is more or less dust in urban households and playgrounds than in
rural environments. Whereas people may breathe the same amount of air, eat and drink the same
amount of food and water, it Is not certain that urban residents consume the same amount of
dust as nonurban. Nevertheless, in the absence of more reliable data, it has been assumed
that urban and nonurban residents consume the same amount of dusts.
The indoor/outdoor ratio of atmospheric lead for urban environments is about 0.8 (Table
7-7). Assuming 2 hours of exposure/day outdoors at a lead concentration of 0.75 pg/m3, 20
hours indoors at 0.6 pg/m3, and 2 hours in a high traffic density area at 5 Mfl/#3. a weighted
mean air exposure of 1.0 Mg/ms appears to be typical of urban residents.
7.3.2.1.2 Houses with interior lead paint. In 1974, the Consumer Product Safety Commission
collected household paint samples and analyzed them for lead content (National Academy of
Sciences; National Research Council, 1976). Analysis of 489 samples showed that 8 percent of
the oil-based paints and 1 percent of the water-based paints contained greater than 0.5
percent lead (5000 pg Pb/g paint, based on dried solids), which was the statutory limit at the
time of the study. The current statutory limit for Federal construction is 0.06 percent. The
greatest amounts of leaded paint are typically found in the kitchens, bathrooms, and bedrooms
(Tyler, 1970; taurer et al., 1973; Gilbert et al., 1979).
Some investigators have shown that flaking paint can cause elevated lead concentrations
In nearby soil. For example, Hardy et al. (1971) measured soil lead levels of 2000 pg/g next
to a barn in rural Massachusetts. A steady decrease in lead level with increasing distance
from the barn was shown, reaching 60 pfl/9 at fifty feet from the barn. Ter Haar (1974)
reported elevated soil lead levels 1n Detroit near eighteen old wood frame houses painted with
lead-based paint. The average soil lead level within two feet of a house was just over 2000
pg/g; the average concentration at ten feet was slightly more than 400 pg/fl- The same author
023PB8/B
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PRELIMINARY DRAFT
reported smaller soil lead elevations in the vicinity of eighteen brick veneer houses in
Detroit. Soil lead levels near painted barns located in rural areas were similar to urban
soil lead concentrations near painted houses, suggesting the importance of leaded paint at
both urban and rural locations. The baseline lead concentration for household dust of 300
pg/g was increased to 2000 pg/g for houses with interior lead based paints. The additional
1700 pg/g would add 85 pg Pb/day to the potential exposure of a child (Table 7-25). This in-
crease would occur in an urban or nonurban environment and would be in addition to the urban
residential increase if the lead-based painted house were in an urban environment.
7.3,2.1.3 Family gardens. Several studies have shown potentially higher lead exposure
through the consumption of home-grown produce from family gardens grown on high lead soils or
near sources of atmospheric lead. Kneip (1978) found elevated levels of lead in leafy vege-
tables, root crops, and garden fruits associated qualitatively with traffic density and soil
lead. Spittler and Feder (1978) reported a linear correlation between soil lead (100 to 1650
pg/g) and leafy or root vegetables. Preer et al. (1980) found a three-fold increase in lead
concentrations of leafy vegetables (from 6 to IS pg/g) in the soil lead range from 150 to 2200
pg/g. In none of these studies were the lowest soil lead concentrations in the normal range
of 10 to 25 pg/g, nor were any lead concentrations reported for vegetables as low as those of
Wolnik et al. (1983) (see Table 7-9).
In family gardens, lead may reach the edible portions of vegetables by deposition of at-
mospheric lead directly on aboveground plant parts or on soil, or by the flaking of lead-
containing paint chips from houses. Traffic density and distance from the road are not good
predictors of soil or vegetable lead concentrations (Preer et al., 1980). Air concentrations
and particle size distributions are the important determinants of deposition on soil or vege-
tation surfaces. Even at relatively high air concentrations (1.5 pg/m3) and deposition velo-
city (0.5 cm/sec) (see Section 6.4.1), it is unlikely that surface deposition alone can
account for more than 2-5 pg/g lead on the surface of lettuce during a 21-day growing period.
It appears that a significant fraction of the lead in both leafy and root vegetables derives
from the soil.
Using the same air concentration and deposition velocity values, a maximum of 1000 pg
lead has been added to each cm2 of the surface of the soil over the past 40 years. With cul-
tivation to a depth of 15 cm, it is not likely that atmospheric lead alone can account for
more than a few hundred pg/g of soil in urban gardens. Urban soils with lead concentrations
of 500 pg/g or more must certainly have another source of lead. In the absence of a nearby
(<5 km) stationary industrial source, paint chips seem the most likely explanation. Even if
the house no longer stands at the site, the lead from paint chips may still be present in the
soil.
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TABLE 7-25. SUMMARY OF POTENTIAL ADDITIVE EXPOSURES TO LEAD
Total
lead
consumed
(pg/day)
Atmospheric
lead
consumed
(pg/day)
Other
lead
sources
(pg/day)
Baseline exposure;
Child
Inhaled air
Food, water & beverages
Oust
0.5
39.9
21.0
0.5
12.1
19.0
27.8
2.0
Total baseline
61.4
31.6
29.8
Additional exposure due to:
Urban atmospheres1
Family gardens2
Interior lead paint3
Residence near smelter4
Secondary occupational8
99
800
85
1300
150
98
200
1300
600
85
Baseline exposure:
Adult male
Inhaled air
Food, water & beverages
Oust
1.0
70.8
4.5
1.0
20.2
2.9
50.6
1.6
Total baseline
76.3
24.1
52.2
Additonal exposure due to:
Urban atmospheres1
28
28
Family gardens2
2000
500
1500
Interior lead paint3
17
17
Residence near smelter4
370
370
Occupational6
1100
1100
Secondary occupational5
21
Smoking
30
27
3
Wine consumption
100
?
?
Hncludes lead from household arid street dust (1000 pg/g) and inhaled air (,75 J•
2assimes soil lead concentration of 2000 pg/g; all fresh leafy and root vegetables, sweet corn
of Table 7-13 replaced by produce from garden. Also assumes 25X of soil lead is of atmos-
pheric origin.
3assumes household dust rises from 300 to 2000 |ig/g. Dust consumption remains the same as
baseline.
^assumes household and street dust increases to 25,000 ng/g.
5assumes household dust increases to 2400 pg/g.
eassumes 8 hr shift at 10 pg Pb/m4 or 90X efficiency of respirators at 100 pg Pb/ra3, and occu-
pational dusts at 100,000 ms/®3-
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Studies of family gardens do not agree on the concentrations of lead in produce. At the
higher soil concentrations, Kneip (1978) reported 0.2 to 1 pg/g in vegetables, Spittler and
Feder (1978) reported 15 to 90 pg/g, and Freer et al. (1980) found 2 to 16 pg/g. Since the
Spittler and Feder (1978) and Preer et al. (1980) studies dealt with soils in the range of
2000 pg/g, these data can be used to calculate a worst case exposure of lead from family
gardens. Assuming 15 pg/g for the leafy and root vegetables [compared to 0.01 to 0.05 pg/g of
the Wolnik et al. (1983) study] family gardens could add 2000 pg/day if the 137 g of leafy and
root vegetables, sweet corn and potatoes consumed by adult males (Table 7-13) were replaced by
family garden products. Comparable values for children and adult females would be 800 and
1600 pg/day, respectively. No conclusive data are available for vine vegetables, but the
ranges of 0.08 to 2 pg/g for tomatoes suggest that the contamination by lead from soil is much
less for vine vegetables than for leafy or root vegetables.
7.3.2.1.4 Houses with lead plumbing. The Glasgow Duplicate Diet Study (United Kingdom
Department of the Environment, 1982) reports that children approximately 13 weeks old living
in houses with lead plumbing consume 6 to 480 pg Pb/day. Water lead levels in the 131 homes
studied ranged from less than 50 to over 500 pg/1. Those children and mothers living in the
homes containing high water-lead levels generally had greater total lead consumption and
higher blood lead levels, according to the study. Breast-fed infants were exposed to much
less lead than bottle-fed infants. Because the project was designed to investigate child and
mother blood lead levels over a wide range of water lead concentrations, the individuals
studied do not represent a typical cross-section of the population. However, results of the
study suggest that infants living in homes with lead plumbing may have exposure to consid-
erable amounts of lead. This conclusion was also demonstrated by Sherlock et al. (1982) in a
duplicate diet study in Ayr, Scotland.
7.3.2.1.5 Residences near smelters and refineries. Air concentrations within 2 km of lead
smelters and refineries average 5 to 15 pg/m3. Assuming the same indoor/outdoor ratio of
atmospheric lead for nonurban residents (0.5), residents near smelters would be exposed to in-
haled air lead concentrations of about 6 pg/m3, compared to 0.05 pg/m3 for the background
levels. Household dust concentrations range from 3000 to 100,000 pg/g (Landrigan et al.,
1975). A value of 25,000 pg/g is assumed for household dust near a smelter. Between inhaled
air and dust, a child 1n this circumstance would be exposed to 1300 pg Pb/day above background
levels. Exposures for adults would be much less, since they consume only 20 percent of the
dusts children consume.
7.3.2.1.6 Occupational exposures. The highest and most prolonged exposures to lead are found
among workers 1n the lead smelting, refining, and manufacturing industries (World Health
Organization, 1977). In all work areas, the major route of lead exposure is by inhalation and
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ingestion of lead-bearing dusts and fumes. Airborne dusts settle out of the air onto food,
water, the workers1 clothing, and other objects, and may be transferred subsequently to the
mouth. Therefore, good housekeeping and good ventilation have a major impact on exposure. It
has been found that levels might be quite high in one factory and low in another solely
because of differences in ventilation, or differences in custodial practices and worker edu-
cation. The estimate of additional exposure on Table 7-25 is for an 8 hour shift at 100 pg
Pb/m3. Occupational exposure under these conditions is primarily determined by occupational
dust consumed. Even tiny amounts (e.g., 10 mg) of dust containing 100,000 pfl Pb/g dust can
account for 1,000 yg/day exposure.
7.3.2.1.6.1 Lead mining, smelting, and refining. Roy (1977) studied exposures during mining
and grinding of lead sulfide at a mill in the Missouri lead belt. Primary smelting operations
were 2.5 miles from the mill, hence the influence of the smelter was believed to be negligible.
The total airborne lead levels were much greater than the concentrations of respirable lead,
indicating a predominance of coarse material.
The greatest potential for high-level exposure exists in the process of lead smelting and
refining (World Health Organization, 1977). The most hazardous operations are those in which
molten lead and lead alloys are brought to high temperatures, resulting in the vaporization of
lead. This is because condensed lead vapor or fume has, to a substantial degree, a small
(respirable) particle size range. Although the total air lead concentration may be greater in
the vicinity of ore-proportioning bins than 1t is in the vicinity of a blast furnace in a
smelter, the amount of particle mass in the respirable size range may be much greater near the
furnace.
A measure of the potential lead exposure in smelters was obtained in a study of three
typical installations in Utah (World Health Organization, 1977). Air lead concentrations near
all major operations, as determined using personal monitors worn by workers, were found to
vary from about 100 to more than 4000 pg/m3. Obviously, the hazard to these workers would be
extremely serious if it were not for the fact that the use of respirators is mandatory in
these particular smelters. Maximum airborne lead concentrations of about 300 pg/m3 were mea-
sured in a primary lead-zinc smelter in the United Kingdom (King et al., 1979). These authors
found poor correlations between airborne lead and blood lead in the smelter workers, and con-
cluded that a program designed to protect these workers should focus on monitoring of biologi-
cal parameters rather than environmental levels.
Spivey et al. (1979) studied a secondary smelter in southern California which recovers
lead mainly from automotive storage batteries. Airborne lead concentrations of 10 to 4800
pg/m3 were measured. The project also involved measurement of biological parameters as well
as a survey of symptoms commonly associated with lead exposure; a poor correlation was found
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between indices of lead absorption and symptom reporting. The authors suggested that such
factors as educational level, knowledge of possible symptoms, and biological susceptibility
may be important factors in influencing symptom reporting. In a second article covering this
same study, Brown et al. (1980) reported that smokers working at a smelter had greater blood
lead levels than nonsmokers. Furthermore, smokers who brought their cigarettes into the work-
place had greater blood lead levels than those who left their cigarettes elsewhere. It was
concluded that direct environmental contamination of the cigarettes by lead-containing dust
may be a major exposure pathway for these individuals (See Section 7.3.2.3.1).
Secondary lead smelters in Memphis, Tennessee and Salt Lake City, Utah were studied by
Baker et al. (1979). The former plant extracted lead principally from automotive batteries,
producing 11,500 metric tons of lead in the eleven months preceding the measurements. The
latter plant used scrap to recover 258 metric tons of lead in the six months preceding the
measurements. Airborne concentrations of lead in the Tennessee study exceeded 200 Mfl/">3 in
some instances, with personal air sampler data ranging from 120 Mg/m3 for a battery wrecker to
350 ug/m3 for two yard workers. At the Utah plant, airborne lead levels in the office, lunch-
room, and furnace room (furnace not operating) were 60, 90, and 100 respectively. When
charging the furnace, the last value increased to 2650 pg/m3. Personal samplers yielded con-
centrations of 17 pg/m3 for an office worker, 700 pg/m3 for two welders, and 2660 pg/m3 f°r
two furnace workers. Some workers in both plants showed clinical manifestations of lead poi-
soning; a significant correlation was found between blood lead levels and symptom reporting.
High levels of atmospheric lead are also found in foundries in which molten lead is al-
loyed with other metals. Berg and Zenz (1967) found in one such operation that average con-
centrations of lead in various work areas were 280 to 600 pg/m3. These levels were sub-
sequently reduced to 30 to 40 pg/m3 with the installation of forced ventilation systems to
exhaust the work area atmosphere to the outside.
7.3.2.1.6.2 Welding and cutting of metals containing lead. When metals that contain lead or
are protected with a lead-containing coating are heated in the process of welding or cutting,
copious quantities of lead in the respirable size range may be emitted. Under conditions of
poor ventilation, electric arc welding of zinc silicate-coated steel (containing 4.5 mg Pb/cm2
of coating) produced breathing-zone concentrations of lead reaching 15,000 Mg/m3, far in
excess of 450 pg/m3, which is the current occupational short-term exposure limit (STEL) in
the United States (Pegues, 1960). Under good ventilation conditions, a concentration of
140 hq/ir3 was measured (Tabershaw et al., 1943).
In a study of salvage workers using oxyacetylene cutting torches on lead-painted struc-
tural steel under conditions of good ventilation, breathing-zone concentrations of lead aver-
aged 1200 pg/m3 and ranged as high as 2400 pg/m3 (Rieke, 1969). Lead poisoning in workers
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dismantling a painted bridge has been reported by Graben et al. (1978). Fischbein et al.
(1978) discuss the exposure of workers dismantling an elevated subway line in New York City,
where the lead content of the paint is as great as 40 percent. The authors report that one
mm3 of air can contain 0.05 g lead at the source of emission. Similarly, Grandjean and Kon
(1981) report elevated lead exposures of welders and other employees in a Baltimore, Maryland
shipyard.
7.3.2.1.6.3 Storage battery industry. At all stages in battery manufacture except for
final assembly and finishing, workers are exposed to high air lead concentrations, particular-
ly lead oxide dust. For example, Boscolo et al. (1978) report air lead concentrations of
16-100 (jg/m3 in a battery factory in Italy, while values up to 1315 yg/m3 have been measured
by Richter et al. (1979) in an Israeli battery factory. Excessive concentrations, as great as
5400 Mi/i"3, have been reported by the World Health Organization (1977).
7.3.2.1.6.4 Printing industry. The use of lead in typesetting machines has declined in
recent years. Air concentrations of 10 to 30 (jg/m3 have been reported where this technique is
used (Parikh et al., 1979). Lead is also a component of inks and dyes used in the printing
industry, and consequently can present a hazard to workers handling these products.
7.3.2.1.6.5 Alkyl lead manufacture. Workers involved in the manufacture of alkyl lead
compounds are exposed to both inorganic and alkyl lead. Some exposure also occurs at the
petroleum refineries where the two compounds are blended into gasoline, but no data are avail-
able on these blenders.
The major potential hazard in the manufacture of tetraethyl lead and tetramethyl lead is
from skin absorption, which is minimized by the use of protective clothing. Linch et al.
(1970) found a correlation between an index of organic plus inorganic lead concentrations in a
plant and the rate of lead excretion in the urine of workers. Significant concentrations of
organic lead in the urine were found in workers involved with both tetramethyl lead and tetra-
ethyl lead; lead levels in the tetramethyl lead workers were slightly higher because the reac-
tion between the organic reagent and lead alloy takes place at a somewhat higher temperature
and pressure than that employed in tetraethyl lead production.
Cope et al. (1979) used personal air .samplers to assess exposures of five alkyl lead
workers exposed primarily to tetraethyl lead. Blood and urine levels were measured over a
six-week period. Alkyl lead levels ranged from 1.3 to 1249 jig/m3, while inorganic lead varied
from 1.3 to 62.6 pg/m3. There was no significant correlation between airborne lead (either
alkyl or inorganic) and blood or urine levels. The authors concluded that biological monito-
ring, rather than airborne lead monitoring, is a more reliable indicator of potential exposure
problems.
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7.3.2.1.6.6 Other occupations. In both the rubber products industry and the plastics
industry there are potentially high exposures to lead. The potential hazard of the use of
lead stearate as a stabilizer in the manufacture of polyvinyl chloride was noted in the 1971
Annual Report of the British Chief Inspector of Factories (United Kingdom Department of
Employment, Chief Inspector of Factories 1972). The inspector stated that the number of
reported cases of lead poisoning in the plastics industry was second only to that in the lead
smelting industry. Scarlato et al. (1969) reported other individual cases of exposure. The
source of this problem is the dust that is generated when the lead stearate is milled and
mixed with the polyvinyl chloride and the plasticizer. An encapsulated stabilizer which
greatly reduces the occupational hazard is reported by Fischbein et al. (1982).
Sakurai et al. (1974), in a study of bioindicators of lead exposure, found ambient air
concentrations averaging 58 pg/*i3 in the lead-covering department of a rubber hose manufactu-
ring plant. Unfortunately, no ambient air measurements were taken for other departments or
the control group.
The manufacture of cans with leaded seams may expose workers to elevated ambient lead
levels. Bishop (1980) reports airborne lead concentrations of 25 to 800 pg/m3 in several can
manufacturing plants in the United Kingdom. Between 23 and 54 percent of the airborne lead
was associated with respirable particles, based on cyclone sampler data.
Firing ranges may be characterized by high airborne lead concentrations, hence instruc-
tors who spend considerable amounts of time in such areas may be exposed to lead. For exam-
ple, Smith (1976) reports airborne lead concentrations of 30 to 160 p/m3 at a firing range in
the United Kingdom. Anderson et al. (1977) discuss lead poisoning in a 17 year old male
employee of a New York City firing range, where airborne lead concentrations as great as 1000
pg/m3 were measured during sweeping operations. Another report from the same research group
presents time-weighted average exposures of instructors of 45 to 900 pg/m3 in three New York
City firing ranges (Fischbein et al., 1979).
Removal of leaded paint from walls and other surfaces in old houses may pose a health
hazard. Feldman (1978) reports an airborne lead concentration of 510 pg/m3, after 22 minutes
of sanding an outdoor post coated with paint containing 2.5 mg Pb/cmz. After only five min-
utes of sanding an indoor window sill containing 0.8 to 0.9 mg Pb/cra2, the air contained 550
pg/m2. Homeowners who attempt to remove leaded paint themselves may be at risk of excessive
lead exposure. Garage mechanics may be exposed to excessive lead concentrations. Clausen and
Rastogi (1977) report airborne lead levels of 0.2 to 35.5 Mfl/m3 in ten garages in Denmark; the
greatest concentration was measured in a paint workshop. Used motor oils were found to con-
tain 1500 to 3500 pg Pb/g, while one brand of unused gear oil contained 9280 pg Pb/g. The
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authors state that absorption through damaged skin could be an important exposure pathway.
Other occupations involving risk of lead exposure include stained glass manufacturing and re-
pair, arts and crafts, and soldering and splicing,
7.3.2.1.7 Secondary occupational exposure. Winegar et al. (1977) examined environmental con-
centrations as well as biological indicators and symptom reporting in workers in a secondary
lead smelter near St. Paul, Minnesota. The smelter recovers approximately 9000 metric tons of
lead per year from automotive batteries. The lead concentrations in cuff dust from trousers
worn by two workers were 60,000 and 600,000 pg/g. The amount of lead contained in pieces of
cloth 1 cm2 cut from the bottoms of trousers worn by the workers ranged from 110 to 3000 pg,
with a median of 410 pg. In all cases, the trousers were worn under coveralls. Dust samples
from 25 households of smelter workers ranged from 120 to 26,000 pg/g, with a median of 2400
pg/g. No significant correlations were found between dust lead concentrations and biological
indicators, or between symptom reporting and biological indicators. However, there was an in-
creased frequency of certain objective physical signs, possibly due to lead toxicity, with in-
creased blood lead level. The authors also concluded that the high dust lead levels in the
workers' homes are most likely due to lead originating in the smelter.
7.3.2.2 Additive Exposure Due to Age, Sex, or Socio-Economic Status.
7.3.2.2.1 Quality and quantity of food. The quantity of food consumed per body weight varies
greatly with age and somewhat with sex. A 14 kg, 2-year-old child eats and drinks 1.5 kg food
and water per day. This is 110 g/kg, or 3 times the consumption of an 80 kg adult male, who
eats 39 g/kg. Teenage girls consume less than boys and elderly women eat more than men, on a
body weight basis.
It is likely that poor people eat less frozen and pre-prepared foods, more canned foods.
Rural populations probably eat more home-grown foods and meats packed locally.
7.3.2.2.2 Mouthing behavior of children. Children place their mouths on dust collecting sur-
faces and lick non-food items with their tongues. This fingersucking and mouthing activity
are natural forms of behavior for young children which expose them to some of the highest con-
centrations of lead in their environment. A single gram of dust may contain ten times more
lead than the total diet of the child.
7.3.2.3 Special Habits or Activities.
7.3.2.3.1 Smoking. Lead is also present in tobacco. The World Health Organization (1977)
estimates a lead content of 2.5 to 12.2 pg per cigarette; roughly two to six percent of this
lead may be inhaled by the smoker. The National Academy of Sciences (1980) has used these
data to conclude that a typical urban resident who smokes 30 cigarettes per day may inhale
roughly equal amounts of lead from smoking and from breathing urban air.
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7.3.2.3.2 Alcoholic beverages. Reports of lead in European wines (Olsen et al., 1981;
Boudene et al., 1975; Zurlo and Graffini, 1973) show concentrations averaging 100 to 200 pg/1
and ranging as high as 300 pg/1. Measurements of lead in domestic wines were in the range of
100 to 300 jjg/1 for California wines with and without lead foil caps. The U.S. Food and Drug
Administration (1983) found 30 pg/1 in the 1982 Market Basket Survey. The average adult con-
sumption of table wine in the U.S. is about 12 g. Even with a lead content of 0.1 pg/g, which
is ten times higher than drinking water, wine does not appear to represent a significant
potential exposure to lead. At one 1/day, however, lead consumption would be greater than the
total baseline consumption.
McDonald (1981) points out that older wines with lead foil caps may represent a hazard,
especially if they have been damaged or corroded. Wai et al. (1979) found that the lead con-
tent of wine rose from 200 to 1200 pg/1 when the wine was allowed to pass over the thin ring
of residue left by the corroded lead foil cap. Hewer wines (1971 and later) use other means
of sealing. If a lead foil is used, the foil is tin-plated and coated with an acid-resistant
substance. Lead levels in beer are generally smaller than those in wine; Thalacker (1980)
reports a maximum concentration of 80 pg/1 in several brands of German beer. The U.S. Food
and Drug Administration (1983) found 13 pg/1 in beer consumed by Americans.
7.3.2.3.3 Pica. Pica is the compulsive, habitual consumption of non-food items, such as
paint chips and soil. This habit can present a significant lead exposure to the afflicted
person, especially to children, who are more apt to have pica. There are very little data on
the amounts of paint or soil eaten by children with varying degrees of pica. Exposure can
only be expressed on a unit basis. Billick and Gray (1978) report lead concentrations of 1000
to 5000 Mfl/cm2 in lead-based paint pigments. A single chip of paint can represent greater ex-
posure than any other source of lead to a child who has pica. A gram of urban soil may have
150 to 2000 pg lead.
7.3.2.3.4 Glazed earthenware vessels. Another potential source of dietary lead poisoning is
the use of inadequately glazed earthenware vessels for 'food storage and cooking. An example
of this danger involved the severe poisoning of a family in Idaho which resulted from drinking
orange juice that had been stored in an earthenware pitcher (Block, 1969). Similar cases,
sometimes including fatalities, have involved other relatively acidic beverages such as fruit
juices and soft drinks, and have been documented by other workers (Klein et al., 1970; Harris
and Elsen, 1967). Because of these incidents, the U.S. Food and Drug Administration (1979)
has established a maximum permissible concentration of 7 pg Pb/g in solution after leaching
with 4 percent acetic acid in the earthenware vessel for 24 hours.
Inadequately glazed pottery manufactured in other countries continues to pose a signifi-
cant health hazard. For example, Spielholtz and Kaplan (1980) report 24 hour acetic
acid-leached lead concentrations as great as 4400 pg/g in Mexican pottery. The leached lead
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decreased with exposure time, and after several days appears to asymptotically approach a
value which may be as great as 600 pg/g. These investigators have also measured excessive
lead concentrations leached into acidic foods cooked for two hours in the same pottery.
Similarly, Acra et al. (1981) report that 85 percent of 275 earthenware vessels produced in
primitive Lebanese potteries had lead levels above the 7 pg/g limit set by the U.S. FDA. How-
ever, only 9 percent of 75 vessels produced in a modern Beirut pottery exceeded the limit.
Cubbon et al. (1981) have examined properly glazed ceramic plates in the United Kingdom, and
have found a decrease in leached lead with exposure time down to very low levels. The authors
state that earthenware satisfying the 7 pg/g limit will contribute about 3 pg/day to the
dietary intake of the average consumer.
7.3.2.3.5 Hobbies. There are a few hobbies where the use of metallic lead or solder may pre-
sent a hazard to the user. Examples are electronics projects, stained glass window construc-
tion, and firing range ammunition recovery. There are no reports in which the exposure to
lead has been quantified during these activities.
7.3.3 Summary of Additive Exposure Factors
Beyond the baseline level of human exposure, additional amounts of lead consumption are
largely a matter of individual choice or circumstance. Many of these additional exposures
arise from the ingestion of atmospheric lead in dust. In one or more ways probably 90 percent
of the American population are exposed to lead at greater than baseline levels. A summary of
the most common additive exposure factors appears on Table 7-25. In some cases, the additive
exposure can be fully quantified and the amount of lead consumed can be added to the baseline
consumption. These may be continuous (urban residence), or seasonal (family gardening) expo-
sures. Some factors can be quantified only on a unit basis because of wide ranges in exposure
duration or concentration. For example, factors affecting occupational exposure are air lead
concentrations (10 to 4000 pg/rn3), use and efficiency of respirators, length of time of expo-
sure, dust control techniques, and worker training in occupational hygiene.
7.4 SUMMARY
Ambient airborne lead concentrations have shown no marked trend from 1965 to 1977. Over
the past five years, however, distinct decreases have occurred. The mean urban air concentra-
tions has dropped from 0.91 pg/m3 in 1977 to 0.32 pg/in3 in 1980. These decreases reflect the
smaller lead emissions from mobile sources in recent years. Airborne size distribution data
indicate that most of the airborne lead mass is found in submlcron particles.
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Atmospheric lead is deposited on vegetation and soil surfaces, entering the human food
chain through contamination of grains and leafy vegetables, of pasture lands, and of soil
moisture taken up by all crops. Lead contamination of drinking water supplies appears to
originate mostly from within the distribution system.
Most people receive the largest portion of their lead intake through foods. Unprocessed
foods such as fresh fruits and vegetables receive lead by atmospheric deposition as well as
uptake from soil; crops grown near heavily traveled roads generally have greater lead levels
than those grown at greater distances from traffic. For many crops the edible internal por-
tions of the plant (e.g., kernels of corn and wheat) have considerably less lead than the
outer, more exposed parts such as stems, leaves, and husks. Atmospheric lead accounts for
about 30 percent of the total adult lead exposure, and 50 percent of the exposure for chil-
dren. Processed foods have greater lead concentrations than unprocessed foods, due to lead
inadvertently added during processing. Foods packaged in soldered cans have much greater lead
levels than foods packaged in other types of containers. About 45 percent of the baseline
adult exposure to lead results from the use of solder lead in packaging food and distributing
drinking water.
Significant amounts of lead in drinking water can result from contamination at the water
source and from the use of lead solder in the water distribution system. Atmospheric deposi-
tion has been shown to increase lead in rivers, reservoirs, and other sources of drinking
water; in some areas, however, lead pipes pose a more serious problem. Soft, acidic water in
homes with lead plumbing may have excessive lead concentrations. Besides direct consumption
of the water, exposure may occur when vegetables and other foods are cooked in water contain-
ing lead.
All of the categories of potential lead exposure discussed above may influence or be in-
fluenced by dust and soil. For example, lead in street dust 1s derived primarily from vehic-
ular emissions, while leaded house dust may originate from nearby stationary or mobile
sources. Food and water may include lead adsorbed from soil as well as deposited atmospheric
material. Flaking leadbased paint has been shown to increase soil lead levels. Natural con-
centrations of lead in soil average approximately 15 pg/g; this natural lead, in addition to
anthropogenic lead emissions, influences human exposure.
Americans living in rural areas away from sources of atmospheric lead consume 50 to 75 pg
Pb/day from all sources. Circumstances which can increase this exposure are: urban residence
(25 to 100 (jg/day), family garden on high-lead soil (800 to 2000 pg/day), houses with interior
lead-based paint (20 to 85 pg/day), and residence near a smelter (400 to 1300 pg/day). Occu-
pational settings, smoking, and wine consumption also can increase consumption of lead accord-
ing to the degree of exposure.
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A number of marinade materials are known to contain lead, the most important being paint
and plastics. Lead-based paints, although no longer used, are a major problem in older hones.
Small children who ingest paint flakes can receive excessive lead exposure. Incineration of
plastics may emit large amounts of lead into the atmosphere. Because of the increasing use of
plastics, this source is likely to become more important. Other manmade materials containing
lead include colored dyes, cosmetic products, candle wicks, and products made of pewter and
silver.
The greatest occupational exposures are found in the lead smelting and refining indus-
tries. Excessive airborne lead concentrations and dust lead levels are occasionally found 1n
primary and secondary smelters; smaller exposures are associated with mining and processing of
the lead ores. Welding and cutting of metal surfaces coated with lead-based paint may also
result in excessive exposure. Other occupations with potentially high exposures to lead in-
clude the manufacture of lead storage batteries, printing equipment, alky! lead, rubber pro-
ducts, plastics, and cans; individuals removing lead paint from walls and those who work in
indoor firing ranges may also be exposed to lead.
Environmental contamination by lead should be measured in terms of the total amount of
lead emitted to the biosphere. American industry contributes several hundred thousand tons of
lead to the environment each year: 35,000 tons from petroleum additives, 50,000 tons from am-
munition, 45,000 tons in glass and ceramic products, 16,000 tons in paint pigments, 8,000 tons
in food can solder, and untold thousands of tons of captured wastes during smelting, refining,
and coal combustion. These are uses of lead which are generally not recoverable, thus they
represent a permanent contamination of the human or natural environment. Although much of
this lead is confined to municipal and industrial waste dumps, a large amount is emitted to
the atmosphere, waterways, and soil, to become a part of the biosphere.
Potential human exposure can be expressed as the concentrations of lead in these environ-
mental components (air, dust, food, and water) that interface with man. It appears that, with
the exception of extraordinary cases of exposure, about 100 (jg of lead are consumed daily by
each American. This amounts to only 8 tons for the total population, or less than 0.01 per-
cent of the total environmental contamination.
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International symposium on the environmental health aspects of lead; October 1972;
Amsterdam, The Netherlands. Luxembourg: Comnission of the European Communities, Centre
for Information and Documentation; pp. 93-98.
E07REF/A
7-86
7/14/83
-------
PRELIMINARY DRAFT
APPENDIX 7A
SUPPLEMENTAL AIR MONITORING INFORMATION
< • u -
7A.1 AIRBORNE LEAD SIZE DISTRIBUTION
In Section 7.2.1.3.1, several studies of the particle s.1ze distributions for atmospheric
lead were discussed. The distributions at forty locations were given In Figure 7-5. Supple-
mentary information from each of these studies 1s given in Table 7A-1.
7A.2 NONURBAN AIR MONITORING INFORMATION
Section 7.2.1.1.1 describes ambient air lead concentrations 1n the United States,
emphasizing monitoring network data from urban stations. Table 7-2 gives the cumulative fre-
quency distributions of quarterly averages for urban stations. Comparable data for nonurban
stations are given 1n Table 7A-2. The trends shown by the two tables are similar, but the
numbers of reports for nonurban stations has decreased markedly since 1977. Table 7A-2 does
not Include nonurban stations located near specific point sources. The detection limit has
decreased over the years, thus there are fewer reports of air concentrations below the
detection limit since 1975.
The distributions of annual averages among specific concentration intervals are given in
Table 7A-3 for nonurban stations. Comparable data were presented graphically in Figure 7-2
for urban stations.
7APPB/B
7A-1
7/1/83
-------
PRELIMINARY DRAFT
TABLE 7A-1.
INFORMATION ASSOCIATED WITH THE AIRBORNE LEAD SIZE
DISTRIBUTIONS OF flGUftt 7-5
Graph
no. Rafarenca
Datas of saapling
Location of saapling
Type of saapler
%
M#/**
Appro*.
MM M>
Lee et a). (1972)
Jan. - Ok. 1970
Average of 4 quarterly
coaposttati swplH,
representing a total of
21 saapling periods of
24 hours each
Chicago, Illinois
IMifiid Anderson
I^MCtor with backup
filter
3.2
0.68
ro
bee et al. (1972)
Lee at al. (1972)
Lea at al. (1972)
Laa at al. (1972)
Laa at al. (1972)
Har. - Dec. 1970
Saae averaging as
Graph 1, total Of IS
saapling period*
Jan. - Dec. 1970
Saae averaging at
Graph 1, total of
21 saapling periods
Har. - Dec. 1970
Saae averaging as
Graph 1, total of 20
saapllne periods
Jan. - Dec. 1970
Saae averaging at
Graph 1, total of 22
saapling periods
Jan. - Dec. 1970
Saae averaging as
Graph 1, total of 23
saapling periods
Cincinnati, Ohio
Denver, Colorado
Philadelphia,
Pennsylvania
St. Louis, Missouri
Washington, D.C.
Modified Andersen 1.8
iapactor with backup
filter
Modified Andersen 1.8
iapactor with backup
filter
Modified Andersen 1.6
iapactor with backup
filter
Modified Andersen 1.8
iapactor with backup
filtar
Modified Andersen 1.3
iapactor with backup
filter
0.48
0.50
0.47
0.69
0.42
-------
PMLIKINARY DRAFT
Graph
no Rafaranca
Datas of saapllng
Lm at «1. (1968)
Saptaabar 1966
Avaraga of 14 runs,
2* hours aach
>
10
U
12
IS
14
Laa at al. (196a)
Padan (1977)
Padaa (1977)
Padan (1977)
CadM (1977)
Parian (1977)
Padan (1977)
Fabruary 1967
Avaraga of 3 runs
4 days aach
Sunar 1975
Avaraga of 4 runs,
avaraga 8 days aach
SuBMr 1972
Avaraga of 3 runt,
avaraga 10 days aach
Sunar 1973
Avaraga of 2 run*
avaraga 5 day* aacti
ar 1973
Avaraga of 2 run*,
avaraga 6 day* aach
Sunar 1972
Avaraga of 9 runs,
avaraga 9 days aach
Sunar 1975
Avaraga of 4 runs,
avaraga 8 days aach
TABU 7A-1. (contlnuad)
% Approx.
Location of saapllng Typa of saaplar PO/a* f*V pa
Cincinnati, Ohio
Fairfax, Ohio
suburb of Cincinnati
Alton, Illinois,
Industrial araa naar
St. Louis
Andarsan t^wctor with 2.8
backup flltar, 1.2s
abova tha ground
Andarsan lapactor with 0.69
backup flltar, 1.2m
above tha ground
Andarsan lapactor
no backup flltar
0.24
0.29
0.42
2.1
Cantraville, Illinois,
downwind of a zinc
saaltar
Andarsan lapactor
with backup flltar
0.62
0.41
Col11nsvilla, Illinois
Industrial araa naar
St. Louis
Andarsan lapactor
with backup flltar
0.67
0.24
KNOX radio transalttar,
Illinois, Industrial
araa naar St. Louis
Andarsan lapactor
with backup flltar
0.60
0.31
Para Narquatta State
Park, Illlonls, upwind
of St. Louis
Andarsan lapactor
with backup flltar
0.15
0.51
Mood Rlvar, Illinois,
Industrial araa naar
St. Louis
Andarsan lapactor,
no backup flltar
0.27
1.8
-------
PRELIMINARY DRAFT
Graph
no taferenca Dates of aaapling
15
U
Choi alt at al.
(1968)
McDonald and
Duncan (1979)
April 1968
average of HMrtl rum,
3 day! each
June 1375
On* run of IS days
^4
3>
17 Dam at al. (1976)
IB Bom at al. (1976)
19 Dailies at al.
(1970)
20 Martens at al.
(1973)
21 Lundgran (1970)
22 Huntzlckar at al.
(1971)
Winter, spring,
mr 1972
Average of 3 runs,
27 day* each
Wintar, spring,
suaatr 1972
Average of 3 runs,
14 days aach
I960
Average of continuous
l-weak runs over an
8-aonlh period
July 1971
Ona run of 4 days
lloveafcer 1968
Average of 10 runs,
16 hours aach
May 1973
Ona run of 8 tiours
TABU 7A-1 (continued)
Location of saapling
Type of saapler
C
T
Mfl/a1
Appro*.
MHO \M
3 sltas: 10,400 and
3300b froa Interstat*
75, Cincinnati, Ohio
Glasgow, Scotland
Southaast Missouri,
800b froa a load
saeltar
Andersen iapactor
with backup f11 tor
Casella iapactor
with backup filter,
30b abova tha ground
Andersen Iapactor,
no backup filter,
1.7a above the ground
7.0*
1.7
1.1
0.53
1.0
0.32
0.51
3.8
Southeast Missouri,
75 las froa the lead
saelter of Graph 17
Andersen Iapactor,
no backup filter,
1.7b above the ground
0.11
2.4
3 sites: 9, 76, and
530a froa U.S. Route 1,
New Brunswick,
Hew Jersey
9 sites throughout
San Francisco area
Riverside, California
Cascade iapactor with
beckup filter
Andersen Iapactor
with backup filter
Lundgren iapactor
4.5
2.2
1.5
0.84
0.59
0.35
0.49
0.50
Shoulder of Pasadena
Freeway near downtown
Los Angelas, California
Andersen iapactor
with backup filter,
2a above the ground
14.0
0.32
-------
PRELIMINARY OMFT
Graph
Reference
Dates of saapllng
23
Huntzickar «t al.
(1975)
Fabruray 1974
On* run of 6 day*
24
Davidson (1977)
Nay and July 1975
Average of 2 runt,
SI How* each
25 Davidson at al.
October 1979
Ona run of 120 hour»
«~i
3>
26
OavldMa at al.
(Utla)
July-Sap. 1979
Average of 2 rune,
90 hour* each
27
Davidson at al.
(lmib)
Oeceataer 1979
Ona run of 52 hours
2a
Goold and
Davidson (1982)
Juna 1900
Ona run of 72 hours
29
Goold and
Davidson (1982)
July 1980
Ona run of 34 hours
TABLE 7A-1 (continued)
Location of sampling
Type of tapler
C
T
MO/"3
Approx.
WO |M
Pasadena, California
Pasadena. California
Cllngaan's Ooae
Great Saokies National
Park, alev. 2024b
Pittsburgh, Pennsylvania
Nepal Himalayas
alev. 3962b
Export, Pennsylvania
rural sit* 40 las
east of Pittsburgh
Packwood, Washington
rural sita in Glfford
Pinchot National Forest
Andersen lapactor 3.5
with backup filter,
on roof of 4 story
building
Modified Andersen 1.2
lapactor with backup
filter on roof of 4
story building
2 Modified Andersen 0,014
lapactors with backup
filters, 1.2* above
the ground
Modified Andersen 0.60
l^xctor with backup
filter, 4b above the
ground
Modified Andersen 0.0014
lapactor with backup
filter, 1.2a above
the ground
2 Modified Andersen 0.1U
lapactors with backup
filters, 1.2a above
the ground
Modified Andersen 0.016
lapactor with backup
filter, 1.5a above
the ground
0.72
0,97
1.0
0.56
0.54
1.2
0.40
I
-------
PRELIMINARY DRAFT
Graph
Reference
Dates of stapling
30 Goold and
Oavidson (1982)
July-Aug. 1980
On* run of 92 hours
31
Dug# at at.
<1976)
May - Juim 1975
One run of 112 hours
32
Ouce at al.
(1976)
July 1S7S
On* run of 79 hours
"»j
>
i
a\
33
34
Harrison at al.
(1971)
Gillette and
Winehestar <1972)
April 1968
Avarago of 21 runs,
2 hours a act)
Oct. 1968
Average of 15 runs,
24 hours cacti
35
Gillette and
Wine ha star <1972)
Kay - $«|>t. 1968
Average of 10 runs,
¦ hours each
36
61I1atta and
Wine hastar <1972)
Oct. 1968
Average of 3 runs,
24 hours each
37
Johansson at al.
(1976)
June - July 1973
Average of 15 runs,
average SO hr each
TABLE 7A-1 (continued)
C
T Approx.
Location of stapling Type of sampler Mfl/*3 MHO m"
Hurricane Ridge
Olyapic National
Park elav. 1600*
Southeast coast of
Berauda
Southeast coast of
Berauda
Ann Arbor, Michigan
Ann Arbor, Michigan
Chicago, Illinois
Modified Andersen 0.0024
iapactor with backup
fiHer, 1.5a above
the ground
Sierra high-voluae O.Q085
iapactor *ith backup
filter, 20a above the
ground
Sierra high-volux 0.0041
Iapactor with backup
filter, 20a above the
ground
Modified Andersen 1.8
iapactor with backup
filter, 20a above the
ground
Andersen iapactor with 0.82
backup filter
Andersen iapactor with 1.9
backup filter
0.87
0.57
0.43
0.16
0.28
0,39
Lincoln, Nebraska
Andersen Iapactor with 0.14
backup filter
0.42
2 sites 1n Tallahassee,
Florida
Oelron Battalia-type 0.24
iapactor, no backup
filter, on building roofs
0.62
-------
PRELIMINARY DRAFT
TABU 7A-1 (continued)
Graph
no
Reference
Dates of saapllng
Location of saapllng
C
T
Type of taapler eg/"*
Approx.
MHO pa
38
Cawse at at.
(1374)
July - Dec. 1973
Chilton, England
Andersen lapactor with 0.16
backup filter, 1.5a above
the ground
0.S7
39
Pattenden et al.
(1974)
Nay - Aug. 1973
Average of 4 runt,
1 aonth each
Trebanos, England
Andersen lapactor with 0.23
backup filter, l.Sa above
the ground
0.74
40
Bernstein and
Rahn (1979)
Aug. 1976
Average of 4 runt,
1 week each
New York City
Cyclone saapling 1.2
systaa with backup
filter, on roof on
IS story building
0.64
"Alrbonn concentration* for filters run at the m sites as tin lapactor, but during different tlx periods. lapactor concentrations not available.
-------
TABLE 7A-2. CUMULATIVE FREQUENCY DISTRIBUTIONS OF QUARTERLY LEAD MEASUREMENTS
AT HONURBAN STATIONS BY YEAR, 1970 THROUGH 1380
(MS/*3)
Percentile Arithmetic Geometric
Std. Std.
Year No. of Minim* 10 30 50 70 90 95 99 Max. Mean dev. Mean dev.
Station qtrly. qtrly.
reports avg. avg.
1970
124
LO
LO
LO
LO
LO
0.267
0.383
0.628
1.471
—
--
—
—
1971
85
LO
LA
LO
LO
LO
0.127
0.204
0.783
1.134
—
—
—
—
1972
137
LO
LO
LO
0.107
0.166
0.294
0.392
0.9S0
1.048
0.139
0.169 0.90
2.59
1973
100
LO
LO
LO
LO
0.132
0.233
0.392
0.698
0.939
—
—
—
—
1974
79
LO
LO
0.053
0.087
0.141
0.221
0.317
0.496
0.534
0.U1
0.111 0.083
2.30
1975
98
LO
LO
LO
LD
0.144
0.255
0.311
0.431
0.649
—
—
—
1976
98
LO
LO
LD
LO
0.105
0.240
0.285
0.336
0.483
—
—
—
—
1977
84
0.006
0.01
0.04
0.08
0.11
0.18
0.20
0.25
0.40
0.09
0.10
0.07
3.19
1978
20
0.002
0.007
0.04
0.06
0.09
0.24
0.33
0.33
0.33
0.08
0.10
0.07
2.84
1979
16
ID
0.02
0.02
0.10
0.14
0.21
0.27
0.32
0.11
0.11
0.13
0.11
3.45
1980
12
U)
0.01
0.005
0.03
0.05
0.11
0.13
0.13
0.13
0.04
0.06
0.05
3.33
Sources: Akland (1976); U.S. Environmental Protection Agency (1978; 1979); Quarterly averages of Lead from NFAN
(1982).
-------
1966
1967
1968
1969
1970-
1971
1972
1973
1974
1975
1976
1977
1978
1979
1980
PRELIMINARY DRAFT
TABLE 7A-3. NUMBER OF NASN NONURBAN STATIONS WHOSE DATA FALL WITHIN
SELECTED ANNUAL AVERAGE LEAD CONCENTRATION INTERVALS, 1966-1980
Concentration interval, pg/m3
<0.03
O
o
-0.096
0.10-0.19
0.20-0.45
Total
No. stations
10
6
3
19
Percent
_
52
32
16
100
No, stations
1
7
10
2
20
Percent
5
35
50
10
100
No. stations
1
15
4
20
Percent
5
75
20
_
100
No. stations
11
9
1
21
Percent
—
52
43
5
100
¦ No. stations
7
3
10
Percent
_
70
30
100
No. stations
10
4
9
11
34
Percent
29
12
26
33
100
No. stations
9
7
6
1
23
Percent
39
31
26
4
100
No. stations
3 ,
q o
5
6
2
16
Percent
19 '
31
38
12
100
No. stations
o"
0
1
4
5
Percent
0
0
20
80
100
No. stations
0
0
3
3
6
Percent
0
0
50
50
100
No. stations
5
8
7
1
21
Percent
24
38
33
5
100
No. stations
1
3
1
0
5
Percent
20
60
20
0
100
No. stations
1
1
1
1
4
Percent
25
25
25
25
100
No. stations
1
2
0
0
3
Percent
33
67
0
0
100
Akland (1976)
; Shearer et al.
(1972);
U.S. Environmental
Protection Agency
(1978;
1979); Annual
averages of lead
fro» NFAN (1982).
7A-9
7/1/83
-------
-------
PRELIMINARY DRAFT
APPENDIX 7B
SUPPLEMENTAL SOIL AND DUST INFORMATION
Lead in soil, and dust of soil origin, 1s discussed in Section 7,2.2. The data show
average soil concentrations are 8 to 25 yg/g, and dust from this soil rarely exceeds 80 to 100
(jg/g. Street dust, household dust and occupational dusts often exceed this level by one to
two orders of magnitude. Tables 7B-1 and 7B-2 summarizes several studies of street dust.
Table 78-3 shows data on household and residential soil dust. These data support the
estimates of mean lead concentrations in dust discussed in Section 7.3.1.4. Table 7B-4 gives
airborne lead concentrations for an occupational setting, which are only qualitatively related
to dust lead concentrations.
7APPB/C
7B-1
7/1/83
-------
PRELIMINARY DRAFT
TABLE 7B-1. LEAD DUST ON AND NEAR HEAVILY TRAVELED ROADWAYS
Sampling site
.Concentration,
MS Pb/g
Reference
Washington, DC:
Busy Intersection
Many sites
Chicago:
Near expressway
Philadelphia:
Near expressway
Brooklyn:
Near expressway
New York City:
Near expressway
Detroit:
Street dust
Philadelphia:
Gutter (low pressure)
Gutter (high pressure)
Miscellaneous U.S. Cities:
Highways and tunnels
Netherlands:
Heavily traveled roads
13,000
4000-8000
6600
3000-8000
900-4900
2000
970-1200
1500
210-2600
3300
280-8200
10,000-20,000
5000
Fritsch and Prival (1972)
Kennedy (1973)
Lombardo (1973}
Plnkerton et al. (1973)
Ter Haar and Aronow (1974)
Shapiro et al. (1973)
Shapiro et al. (1973)
Buckley et al, (1973)
Raneau (1973)
TABLE 7B-2. LEAD CONCENTRATIONS IN STREET DUST IN
LANCASTER, ENGLAND
No. of Range of Standard
Site samples concentrations Mean deviation
Car parks
4
39,700 -
51,900
46,300
5,900
16
950 -
15,000
4,560
3,700
Garage forecourts
2
44,100 -
48,900
46,500
—
7
1,370 -
4,480
2,310
1,150
Town centre streets
13
840 -
4,530
2,130
960
Main roads
19
740 -
4,880
1,890
1,030
Residential areas
7
620 -
1,240
850
230
Rural roads
4
410 -
870
570
210
Source: Harrison (1979).
7APPB/C 7B-2 7/1/83
-------
PRELIMINARY DRAFT
TABLE 7B-3. LEAD- DUST IN RESIDENTIAL AREAS
Sampling site
Concentration,
|jg Pb/g
Reference
Philadelphia:
Classroom
Playground
Window frames
Boston and New York:
House dust
Brattleboro, VT:
In home
New York City:
Middle Class
Residential
Philadelphia:
Urban industrial
Residential
Suburban
Derbyshire, England:
Low soil lead area
High soil lead area
2000
3000
1750
1000-2000
500-900
610-740
3900
930-16,000
610
290-1000
830
280-1500
520
130-3000
4900
1050-28,000
Shapiro et al. (1973)
Needleman and Scanlon (1973)
Darrow and Schroeder (1974)
Pinkerton et al. (1973)
Needleman et al. (1974)
Needleman et al. (1974)
Needleman et al. (1974)
Barltrop et al. (1975)
Barltrop et al. (1975)
TABLE 7B-4. AIRBORNE LEAD CONCENTRATIONS BASED ON PERSONAL SAMPLERS, WORN BY
EMPLOYEES AT A LEAD MINING AND GRINDING OPERATION IN THE MISSOURI
LEAD BELT
Air lead concentration (pg/ii3)
Occupation
High
Low
Mean
Mill operator
flotation operator
Filter operator
Crusher operator
Sample finisher
Crusher utility
Shift boss
Equipment operator
6
300
50
180
4
750
100
320
4
2450
380
1330
4
590
20
190
2
10,000
7070
8530
1
—
—
70
5
560
110
290
1
—
—
430
N denotes number of air samples.
Source: Roy (1977).
7APP8/C
7B-3
7/1/83
-------
-------
PRELIMINARY DRAFT
APPENDIX 7C
STUDIES OF SPECIFIC POINT SOURCES
OF LEAD
This collection of studies 1s Intended to extend and detail the general picture of lead
concentrations 1n proximity to Identified major point sources as portrayed 1n Chapter 7.
Because emissions and control technology vary between point sources, each point source 1s
unique in the degree of environmental contamination. The list is by no means all-inclusive,
but Is intended to be representative and to supplement the data cited in Chapter 7. In many
of the studies, blood samples of workers and their families were taken. These studies are
also discussed in Chapter 11.
7C.1 SMELTERS AND MINES
7C.1.1 Two Smelter Study
The homes of workers of two unidentified secondary lead smelters in different geograph-
ical areas of the United States were studied by Rice et al. (1978). Paper towels were used to
collect dust from surfaces in each house, following the method of Vostal et al. (1974). A
total of 33 homes of smelter workers and 19 control homes located in the same or similar
neighborhoods were investigated. The geometric mean lead levels on the towels were 79.3 pg
(smelter workers) versus 28.8 pg (controls) 1n the first area, while In the second area mean
values were 112 pg versus 9.7 pg. Also in the second area, settled dust above doorways was
collected by brushing the dust Into glassine envelopes for subsequent analysis. The geometric
mean lead content of this dust in 15 workers' homes was 3300 pg/g, compared with 1200 pg/g
in eight control homes. Curbslde dust collected near each home 1n the second area had a
geometric mean lead content of 1500 pg/g, with no significant difference between worker and
control homes. No significant difference was reported in the paint lead content between
worker and control homes. The authors concluded that lead 1n dust carried home by these
workers contributed to the lead content of dust 1n their homes, despite showering and changing
clothes at the plant, and despite work clothes being laundered by the company. Storage of
employee street clothes in dusty lockers, walking across lead-contaminated areas on the way
home, and particulate settling on workers' cars in the parking lot may have been important
factors. Based on measurement of zinc protoporphyrin levels 1n the blood of children in these
homes, the authors also concluded that the greater lead levels in housedust contributed to In*
creased child absorption of lead.
7APPB/D
7C-1
7/1/83
-------
PRELIMINARY DRAFT
7C.1.2 British Columbia. Canada
Neri et al. (1978) and Schmitt et al. (1979) examined environmental lead levels in the
vicinity of a lead-zinc smelter at Trail, British Columbia. Total emissions from the smelter
averaged about 135 kg Pb/day. Measurements were conducted in Trail (population 12,000), in
Nelson, a control city 41 kilometers north of Trail (population 10,000), and in Vancouver.
The annual mean airborne lead concentrations in Trail and in Nelson were 2.0 and 0.S yg/na,
respectively. Mean lead levels In surface soil were 1320 Mfl/fl 1n Trail (153 samples), 192
Mg/g in Nelson (55 samples), and 1545 ng/g in Vancouver (37 samples).
Blood lead measurements shows a positive correlation with soil lead levels for children
aged 1-3 years and for first graders, but no significant correlation for ninth graders. The
authors concluded that small children are most likely to ingest soil dust, and hence deposited
smelter-emitted lead may pose a potential hazard for the youngest age group.
7C.1.3 Nether!ands
Environmental lead concentrations were measured 1n 1978 near a secondary lead smelter in
Arnhem, Netherlands (Diemel et al., 1981). Air and dust were sampled in over 100 houses at
distances of 450 to 1000 meters from the smelter, with outdoor samples of air, dust, and soil
collected for comparison. Results are presented in Table 7C-1. Note that the mean indoor
concentration of total suspended particulates (TSP) is greater than the mean outdoor concen-
tration, yet the mean indoor lead level is smaller than the corresponding outdoor level. The
authors reasoned that indoor sources such as tobacco smoke, consumer products, and decay of
furnishings are likely to be Important in affecting indoor TSP; however, much of the indoor
lead was probably carried in from the outside by the occupants, e.g., as dust adhering to
shoes. The Importance of resuspenslon of indoor particles by activity around the house was
also discussed.
7C.1.4 Belgium
Roels et al. (1978; 1980) measured lead levels in the air, in dust, and on childrens'
hands at varying distances from a lead smelter 1n Belgium (annual production 100,000 metric
tons}. Blood data from children living near the smelter were also obtained. A1r samples were
collected nearly continuously beginning in September 1973. Table 7C-2 lists the airborne con-
centrations recorded during five distinct population surveys between 1974 and 1978, while
Figure 7C-1 presents air, dust, and hand data for Survey #3 in 1976. Statistical tests showed
that blood lead levels were better correlated with lead on childrens" hands than with air
lead. The authors suggested that Ingestion of contaminated dust by hand-to-mouth activities
7APPB/0
7C-2
7/1/83
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PRELIMINARY DRAFT
such as nail-biting and thumb-sucking, as well as eating with the hands, may be an Important
exposure pathway. It was concluded that Intake fro* contamlnated hands contributes at least
two to four tines as much lead as Inhalation of airborne material.
TABLE 7C-1. LEAD CONCENTRATIONS IN INDOOR AND OUTDOOR AIR, INDOOR AND OUTDOOR
DUST, AND OUTDOOR SOIL NEAR THE ARNHEM, NETHERLANDS SECONDARY LEAD SMELTER
(INDOOR CONCENTRATIONS)
Arithmetic
*
Parameter
mean
Range
n
Suspended particulate matter
dust concentration (yg/m8)
140
20-570
101
lead concentration (yg/ms)
0.27
0.13-0.74
101
dust lead content (yg/kg)
2670
400-8200
106
Dustfal1
dust deposition (mg/m8»day)
15.0
1.4-63.9
105
lead deposition (pg/m^day)
9.30
1.36-42.4
105
dust lead content (mg/kg)
1140
457-8100
105
Floor dust
amount of dust (mg/nt8)
356
41-2320
107
amount of lead (pg/ma)
166
18-886
101
Dust lead content (mg/kg)
in "fine" floor dust
1050
463-4740
107
in "coarse" floor dust
370
117-5250
101
*N number of houses.
(OUTDOOR CONCENTRATIONS)
Parameter
Arithmetic mean
Range
Suspended particles
dust concentration
lead concentraton (tjg/m*)
(high-volume samplers, 24-hr
samples, 2 months' average)
Lead in dustfall
(yg/m^day)
(deposit gauges, weekly
samples, 2 months' average)
Lead in soil
(mg/kg 0-5 cm)
Lead In streetdust
(mg/kg <0.3 mm)
54.5
0.42
508
322
860
53.7-73.3
0.28-0.52
208-2210
21-1130
77-2670
Source: Dlemel et al (1981).
7APPB/D
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Pb IN AIR
n> IN DUST
Pb ON HAND L
0
1
Z
a
1
1
1
1
0
7M
in
•et
1
1
1
I
0
1(0
too
«o
M/hand
AT LESS THAN 1km FROM LEAD SMELTER
1
20 9
AT » km FROM LEAD SMELTER
URBAN - BRUSSELS
RURAL - HERENT
CHILDREN 1171
3RD SURVEY
Figure 7C-1. Concentration* of lead In air. In dual, and on children's hands, measured
during the third population survey of Table E. Values obtained less than 1 km from the
smelter, at 2.5 km from the smelter, and in two control areas are shown.
Source: Roels et al. (1980).
7APPB/0
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PRELIMINARY DRAFT
TABLE 7C-2. AIRBORNE CONCENTRATIONS OF LEAD DURING FIVE
POPULATION SURVEYS NEAR A LEAD SHELTER IN BELGIUM*
Pb-A1r
Study populations (Mg/m8)
1 Survey
<1 km
4.06
(1974)
2.5 km
1.00
Rural
0.29
2 Survey
<1 km
2.94
(1975)
2.5 km
0.74
Rural
3 Survey
<1 kra
3.67
(1976)
2.5 km
0.80
Urban
0.45
Rural
0.30
4 Survey
<1 km
3.42
(1977)
2.5 km
0.49
5 Survey
<1 km
2.68
(1978)
2.5 km
0.54
Urban
0.56
Rural
0.37
"Additional airborne data 1n rural and urban areas obtained as controls are also shown.
Source: Roels et al. (1380).
7C.1.5 Meza River Valley. Yugoslavia
In 1967, work was Initiated 1n the community of Zerjav, situated 1n the Slovenian Alps on
the Meza River, to Investigate contamination by lead of the air, water, snow, soil, vegeta-
tion, and animal life, as well as the human population. The mselter in this community pro-
duces about 20,000 metric tons of lead annually; until 1969 the stack emitted lead oxides
without control by filters or other devices. Five sampling sites with high-volume samplers
operating on a 24-hr basis were established in the four principal settlements Within the Meza
River Valley (Figure 7C-2): (1) Zerjav, in the center, the site of the smelter, housing 1503
inhabitants, (2) Rudarjevo, about 2 km to the south of Zerjav with a population of 100;
(3) Crna, some 5 kit to the southwest, population 2198, where there are two sites (Crna-SE and
Crna-W); and (4) Mezica, a village about 10 km to the northwest of the smelter with 2515
7APP8/Q
7C-5
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PRELIMINARY DRAFT
Inhabitants. The data 1n Table 7C-3 are sufficient to depict general environmental contami-
nation of striking proportions.
7C.X.6 Kosova Province. Yuaoslavla
Popovac et al. (1982) discuss lead exposure in an industrialized region near the town of
Kosova Mitrovica, Yugoslavia, containing a lead smelter and refinery, and a battery factory.
In 1979, 5800 kg of lead were emitted daily from the lead smelter alone. Ambient air concen-
trations in the town were in the range 21.2 to 29.2 yg/m3 In 1980, with levels occasionally
reaching 70 pg/ms. The authors report elevated blood lead levels in most of the children
tested; some extremely high values were found, suggesting the presence of congenital lead
poisoning.
7C.1.7 Czechoslovakia
Wagner et al. (1981) measured total suspended particulate and airborne lead concentra-
tions in the vicinity of a waste lead processing plant in Czechoslovakia. Data are shown in
Table 7C-4. Blood lead levels in 90 children living near the plant were significantly greater
than in 61 control children.
7C.1.8 Australia
Heyworth et al. (1981) examined child response to lead in the vicinity of a lead sulfide
mine in Northhampton Western Australia. Two samples of mine tailings measured in 1969
contained 12,000 pg/g and 28,000 pg/g lead; several additional samples analyzed in 1978 con-
tained 22,000 pg/g to 157,000 pg/g lead. Surface soil from the town boundry contained 300
pg/g, while a playground and a recreational area had soil containing 11,000 pg/g and 12,000
pg/g lead respectfully.
Blood lead levels measured in Northhaaptom children, near the mine, were slightly greater
than levels measured 1n children living a short distance away. The Northhampton blood lead
levels were also slightly greater than those reported for children in Victoria, Australia
(DeSilva and Donnan, 1980). Heyworth et al. concluded that the mine tailings could have
increased the lead exposure of children living in the area.
7C.2 BATTERY FACTORIES
7C.2.1 Southern Vermont
Watson et al. (1978) Investigated homes of employees of a lead storage battery plant in
southern Vermont In August and September, 1976. Lead levels in household dust, drinking
water, and paint were determined for 22 workers' horns and 22 control homes. The mean lead
7APPB/D 7C-6 7/1/83
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mi in *
O 9*i I Tf*t; nANT
StmiHiNTS
Figure 7C-2. Schematic plan of lead mine and smelter from Meza Valley,
Yugoslavia, study.
Source: Fugas (1977).
7APPB/D
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PRELIMINARY DRAFT
Table 7C-3. ATMOSPHERIC LEAD CONCENTRATIONS (24-hour) IN THE
MEZA VALLEY, YUGOSLAVIA, NOVEMBER 1971 TO AUGUST 1972
Site
Pb concentration, itg/m3
Minimum
Maximum
Average
Mezlca
0.1
236.0
24.2
Zerjav
0.3
216.5
29.5
Rudarjevo
0.5
328.0
38.4
Crna SE
0.1
258.5
33.7
Crna W
0.1
222.0
28.4
Source: Fugas (1377).
TABLE 7C-4. CONCENTRATIONS OF TOTAL AIRBORNE OUST AND OF AIRBORNE LEAD IN THE
VICINITY OF A WASTE LEAD PROCESSING PLANT IN CZECHOSLOVAKIA,
AND IN A CONTROL AREA INFLUENCED PREDOMINANTLY BY AUTOMOBILE EMISSIONS
TSP Lead
Exposed
n
300
303
x (Mfl/"8)
113.6
1.33
S
83.99
1.9
range
19.7-553.4
0.12-10.9
95% c.1.
123.1-104.1
1.54-1.11
Control
n
56.0
87
x (m8/«i3)
92.0
0.16
S
40.5
0.07
range
10-210
0.03-0.36
95* c.1.
102.7-81.3
0.17-0.14
n ¦ nunber of samples; x *= mm of 24-hour samples;
s * standard deviation; 95X confidence Interval.
Source: Wagner et al. (1981).
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PRELIMINARY DRAFT
concentration In dust In the workers' homes was 2,200 nfl/fl. compared with 720 M9/9 In the
control hones. Blood lead levels in the workers' children wire greater than levels 1n the
control children, and were significantly correlated with dust lead concentrations. No sig-
nificant correlations were found between drinking water lead and blood lead, or between paint
lead and blood lead. It is noteworthy that although 90 percent of the employees showered and
changed clothes at the plant, 87 percent brought their work clothes home for laundering. The
authors concluded that dust carried home by the workers contributed to increased lead absorp-
tion in their children.
7C.2.2 North Carolina
Several cases of elevated environmental lead levels near point sources in North Carolina
have been reported by Dolcourt et al. (1978; 1981). In the first instance, dust lead was
measured in the homes of mothers employed 1n a battery factory in Raleigh; blood lead levels
in the ntothers and their chldren were also measured. Carpet dust was found to contain 1,700
to 48,000 Hfl/g lead in six homes where the children had elevated blood lead levels (>40
Mg/dl). The authors concluded that lead carried home on the mothers' clothing resulted In
Increased exposure to their children (Dolcourt et al., 1978). In this particular plant, no
uniforms or garment covers were provided by the factory; work clothing was worn home.
In a second case, discarded automobile battery casings from a small-scale lead recovery
operation in rural North Carolina were brought home by a worker and used in the family's
wood-burning stove (Oolcourt et al,, 1981). Two samples of indoor dust yielded 13,000 and
41,000 Mg/g lead. A three-year-old girl living 1n the house developed encephalopathy
resulting in permanent brain damage.
In a third case, also in rural North Carolina, a worker employed in an automobile battery
reclamation plant was found to be operating an illicit battery recycling operation 1n his
home. Reclaimed lead was melted on the kitchen stove. Soil samples obtained near the house
measured as high as 49 percent lead by weight; the driveway was covered with fragments of
battery casings. Although no family member had evidence of lead poisoning, there were
unexplained deaths among chickens who fed where the lead waste products were discarded
(Oolcourt et al., 1981).
7C.2.3 Oklahoma
Morton et al. (1982) studied lead exposure in children of employees at a battery manu-
facturing plant in Oklahoma. A total of 34 lead-exposed children and 34 control children were
examined during February and March, 1978; 18 children 1n the lead-exposed group had elevated
blood lead levels (>30 yg/dl), while none of the controls were in this category.
7APPB/D
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7/1/83
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PRELIMINARY DRAFT
It was found that many of the battery factory employees also used lead at home, such as
casting lead Into fishing sinkers and using leaded ammunition. A significant difference in
blood lead levels between the two groups of children was found even when families using lead
at hone were deleted from the data set. Using the results of personal Interviews with the
homenaker in each household, the authors concluded that dust carried home by the employees
resulted in increased exposure of their children. Merely changing clothes at the plant was
deemed insufficient to avoid transporting appreciable amounts of lead home: showering and
shampooing, in addition to changing clothes, was necessary.
7C.2.4 Oakland. California
Environmental lead contamination at the former site of wet-cell battery manufacturing
plant in Oakland, California was reported by Wesolowski et al. (1979). The plant was opera-
tional from 1924 to 1974, and was demolished in 1976. Soil lead levels at the site measured
shortly after demolition are shown in Table 7C-5. The increase in median concentrations with
depth suggested that the battery plant, rather than emissions from automobiles, were respons-
ible for the elevated soil lead levels. The levels decreased rapidly below 30 cm depth. The
contaminated soil was removed to a sanitary landfill and replaced with clean soil; a park has
subsequently been constructed at the site.
TABLE 7C-5. LEAD CONCENTRATIONS IN SOIL AT THE FORMER SITE OF A WET-CELL
BATTERY MANUFACTURING PLANT IN OAKLAND, CALIFORNIA
Depth
N
Range
Mean
Median
(ug/o)
(Mfl/fl)
(Mfl/fl)
Surface
24
57-96,000
4300
200
15 cm
23
13-4200
370
200
30 on
24
13-4500
1100
360
Source: Wesolowski et al. (1979),
7C.2.5 Manchester. England
Elwood et al. (1977) measured lead concentrations in air, dust, soil, vegetation, and tap
water, as well as 1n the blood of children and adults, in the vicinity of a large battery
factory near Manchester. It was found that lead levels 1n dust, soil, and vegetation
decreased with Increasing distance from the factor. Airborne lead concentrations did not show
a consistent effect with downwind distance, although higher concentrations were found downwind
7APPB/D
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7/1/83
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PRELIMINARY ORAFT
compared with upwind of the factor. Blood lead levels were greatest 1n the households of
battery factor employees: other factors such as distance from the factory, car ownership, age
of house, and presence of lead water pipes were outweighed by the presence of a leadworker in
the household. These results strongly suggest that lead dust carried home by the factor
employees 1s a dominant exposure pathway for their families. The authors also discussed the
work of Burrows (1976), who demonstrated experimentally that the nost important means of lead
transport from the factory into the home is via the workers' shoes.
7APPB/D
7C-11
7/1/83
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PRELIMINARY DRAFT
APPENDIX 7D
SUPPLEMENTAL DIETARY INFORMATION FROM THE
U.S. FDA TOTAL OIET STUDY
The U.S. Food and Drug Administration published a new Total Diet Food List (Pennington,
1983) based on over 100,000 dally diets from 50,000 participants. Thirty five hundred
*
categories of foods were condensed to 201 adult food categories for 8 age/sex groups.
Summaries of these data were used in Section 7.3.1.2 to arrive at lead exposures through food,
water, and beverages. For brevity and continuity with the crop data of Section 7.2.2.2.1, it
was necessary to condense the 201 categories of the Pennington study to 25 categories in this
report.
The preliminary lead concentrations for all 201 items of the food list were provided by
U.S. Food and Drug Administration (1983). These data represent three of the four Market
Basket Surveys, the fourth to be provided at a later time. Means of these values have been
calculated by EPA, using one-half the detection limit for values reported below detection
limit. These data appear in Table 7D-1.
In condensing the 201 categories of Table 70-1 to the 25 categories of Table 7-15,
coatbinations and fractional combinations of categories were made according to the scheme of
Table 7D-2. In this way, specific categories of food more closely identified with farm
products were summarized. The assumptions made concerning the ingredients In the final
product, (mainly water, flour, eggs, and milk) had little influence on the outcome of the
summarization.
7APPB/E
7D-1
7/1/83
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2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44
PRELIMINARY DRAFT
TABLE 7D-1. FOOD LIST AND PRELIHINARY LEAD CONCENTRATIONS
Food Lead concentration* Mean*
(Mfl/fl)
Whole milk
0.01
Low fat milk
0.02
T
T
0.017
Chocolate milk
0.04
0.02
Skim milk
0.01
Butter milk
0.01
Yogurt, plain
0.01
Milkshake
0.06
0.05
0.04
Evaporated nllk
0.08
0.07
0.18
0.11
Yogurt, sweetened
0.04
0.02
Cheese, American
0.03
0.97
Cottage cheese
0.05
0.023
Cheese, Cheddar
0.04
0.020
Beef, ground
0.11
0.043
Beef, chuck roast
0.09
0.03
0.043
Beef, round steak
0.01
Beef, sirloin
0.01
Pork, ham
0.03
0.017
Pork chop
0.03
0.017
Pork sausage
0.03
0.05
0.030
Pork, bacon
0.05
0.22
0.093
Pork roast
0.01
Lamb chop
0.03
0.017
Veal cutlet
0.01
Chicken, fried
0.04
0.020
Chicken, roasted
o.oi •
Turkey, roasted
0.01
Beef liver
0.11
0.12
0.08
Frankfurters
0.01
Bologna
0.02
0.013
Salami
0.01
Cod/haddock filet
0.07
0.03
Tuna, canned
0.18
0.27
0.08
0.18
Shrimp
0.10
0.04
Fish sticks, frozen
0.03
0.017
Eggs, scrambled
0.01
Eggs, fried
0.03
0.017
Eggs, soft boiled
0.01
Pinto beans, dried
0.04
0.02
0.023
Pork and beans, canned
0.41
0.07
0.04
0.17
Cowpeas, dried
0.01
Lima beans, dried
0.03
0.017
Lima beans, frozen
0.03
0.017
Navy beans, dried
0.03
0.017
Red beans, dried
0.02
0.06
0.03
7D-2
^ •
-------
45
46
47
48
49
50
51
52
53
54
55
56
5?
58
59
60
61
62
63
64
65
66
67
68
69
70
71
72
73
74
75
76
77
78
79
80
81
82
83
84
85
86
87
88
89
90
91
92
93
PRELIMINARY ORAFT
TABLE 70-1. (continued)
Food Lead concentration* Mean*
(mo/q)
Peas, green, canned
0.14
0.28
0.25
0.22
Peas, green, frozen
0.03
0.08
0.04
Peanut butter
0.15
0.56
Peanuts
0.01
Pecans
0.03
0.017
Rice, white
0.05
0.19
0.084
Oataeal
0.06
0.027
Farina
0.03
0.017
Corn grits
0.01
Corn, frozen
T
T
.
0.013
Corn, canned
0.22.
0.16
0.06
0.28
Corn, cream style, canned
0.09
0.06
0.11
0.09
Popcorn
0.07
0.08
0.053
White bread
0.01
Rolls, white
0.03
0.06
0.02
0.037
Cornbread
0.01
Biscuits
0.04
0.02
0.023
Whole wheat bread
0.05
0.03
0.03
Tortilla
0.02
0.03
0.02
0.023
Rye bread
0.03
0.02
0.02
Muffins
0.01
Crackers, sal tine
0.03
0.017
Corn chips
0.04
0.02
Pancakes
0.03
0.017
Noodles
0.04
0.05
0.033
Macaroni
0.02
0.013
Corn flakes
0.04
0.02
Pre-sweetened cereal
0.06
0.03
0.033
Shredded wheat cereal
0.01
Raisin bran cereal
0.03
0.017
Crisped rice cereal
0.02
0.013
Granola
0.03
0.02
0.02
Oat ring cereal
0.03
0.02
0.04
0.03
Apple, raw
0.04
0.04
0.03
Orange, raw
0.03
0.02
0.02
Banana, raw
0.01
Watermelon, raw
0.02
0.013
Peach, canned
0.18
0.23
0.28
0.23
Peach, raw
0.02
0.04
0.023
Applesauce, canned
0.21
0.19
0.10
0.17
Pear, raw
0.02
0.03
0.02
Strawberries, raw
0.03
0.017
Fruit cocktail, canned
0.23
0.24
0.13
0.20
Grapes, raw
0.02
0.013
Cantaloupe, raw
0.03
0.08
0.04
Pear, canned
0.24
0.22
0.17
0.31
Pluns, raw
T
0.012
Grapefruit, raw
0.03
0.017
Pineapple, canned
0.10
0.08
0.05
0.08
70-3
7/1/83
-------
Cati
94
95
96
97
98
99
100
101
102
103
104
105
106
107
108
109
110
111
112
113
114
115
116
117
118
119
120
121
122
123
124
125
126
127
128
129
130
131
132
133
134
135
136
137
138
139
140
141
142
143
PRELIMINARY DRAFT
TABLE 70-1. (continued)
M^PMM55BB5g5B5HBWMIIW—WWI 'I Till i'i'' . IT 1 , J." ¦ I.I *n L'i "
Food Lead concentration* Mean
(MS/9)
Cherries, raw
0.03
0.017
Raisins, dried
0.04
0.04
0.03
Prunes, dried
0.05
0.04
0.033
Avocado, raw
0.03
0.07
0.037
Orange juice, frozen
0.02
0.013
Apple juice, canned
0.06
0.09
0.02
0.054
Grapefruit juice, frozen
0.03
0.04
0.027
Grape juice, canned
0.06
0.11
0.04
0.07
Pineapple juice, canned
Prune juice, bottled
0.08
0.02
0.05
0.05
0.02
0.02
0.017
Orange juice, canned
0.05
0.03
0.02
0.033
Lemonade, frozen
0.04
0.07
0.03
Spinach, canned
0.80
1.65
0.12
0.86
Spinach, frozen
0.05
0.10
0.06
0.07
Col lards, frozen
0.05
0.27
0.04
0.12
Lettuce, raw
0.01
Cabbage, raw
0.03
0.017
Coleslaw
0.13
0.05
Sauerkraut, canned
0.77
0.39
0.12
0.43
Broccoli, frozen
0.04
0.03
0.027
Celery, raw
0.01
Asparagus, frozen
0.02
0.013
Cauliflower, frozen
0.01
Tomato, raw
0.03
0.017
Tomato juice, canned
0.16
0.04
T
0.072
Tomato sauce, canned
0.26
0.31
0.12
0.23
Tomatoes, canned
0.19
-
0.23
0.21
Beans, snap green, frozen
0.03
0.02
0.02
Beans, snap green, canned
0.14
0.23
0.12
0.16
Cucumber, raw
T
0.012
Squash, summer, frozen
0.04
0.02
0.023
Pepper, green, raw
0.07
0.02
0.033
Squash, winter, frozen
0.02
0.013
Carrots, raw
0.03
0.017
Onion, raw
0.05
0.02
0.027
Vegetables, nixed, canned
0.17
0.06
0.08
Mushroons, canned
0.25
0.25
0.12
0.21
Beets, canned
0.17
0.11
0.08
0.12
Radish, raw
0.03
0.03
0.023
Onion rings, frozen
0.07
0.02
0.033
French fries, frozen
T
0.012
Mashed potatoes, instant
0.11
0.043
Boiled potatoes, w/o peel
0.02
0.013
Baked potato, w/ peel
0.04
0.02
0.023
Potato chips
0.03
0.017
Scalloped potatoes
0.04
0.02
0.023
Sweet potato, baked
0.05
0.04
0.033
Sweet potato, candied
0.04
0.04
0.02
0.033
Spaghetti, w/ meat sauce
0.11
0.12
0.08
0.10
Beef and vegetable stew
T
0.012
7D-4
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PRELIMINARY DRAFT
TABLE 70-1. (continued)
Category
Food
Lead concentration*
(MS/fl)
Means*
144
Pizza, frozen
0.06
0.03
0.033
145
Chili, beef and beans
0.12
0.05
0.06
146
Macaroni and cheese
0.01
147
Hamburger sandwich
0.02
0.013
148
Meatloaf
0.06
0.46
0.17
149
Spaghetti 1n tomato sauce.
canned
0.06
0.02
0.03
150
Chicken noodle casserole
0.04
0.02
151
Lasagne
0.11
0.06
0.03
0.067
152
Potpie, frozen
0.04
0.03
0.027
153
Pork chow mein
0.32
0.03
0.04
0.13
154
Frozen dinner
0.01
155
Chicken noodle soup, canned 0.02
0.02
0.06
0.033
156
Tomato soup, canned
0.07
0.02
T
0.035
157
Vegetable beef soup, canned
0.04
0.04
0.04
0.04
158
Beef bouillon, canned
0.02
0.013
159
Gravy mix
0.02
0.013
160
White sauce
0.05
0.02
0.027
161
Pickles
0.10
0.09
0.67
162
Margarine
0.06
0.06
0.043
163
Salad dressing
0.03
0.06
0.033
164
Butter
0.14
0.053
165
Vegetable oil
0.01
166
Mayonnai se
0.01
167
Cream
0.06
0.027
168
Cream substitute
0.10
0.04
0.05
169
Sugar
0.07
0.05
0.043
.170
Syrup
0.06
0.027
171
Jelly
0.05
0.023
172
Honey
0.12
0.06
0.063
173
Catsup
0.02
0.013
174
Ice cream
0.03
0.02
0.03
0.027
175
Pudding, instant
0.01
176
Ice cream sandwich
0.05
0.02
0.027
177
Ice milk
0.07
0.04
0.02
0.043
178
Chocolate cake
0.13
0.03
0.057
179
Yellow cake
0.16
0.06
180
Coffee cake
0.04
0.03
0.05
0,04
181
Doughnuts
0.02
0.013
182
Danish pastry
0.06
0.037
183
Cookies, choc, chip
0.04
0.03
0.03
0.033
184
Cookies, sandwich type
0.03
0.03
0.04
0.027
185
Apple pie, frozen
0.04
0.02
0.023
186
Pumpkin pie
0.05
0.02
0.03
0.033
187
Candy, Bilk chocolate
0.09
0.04
0.09
0.07
188
Cancjy, caramels
0.04
0.04
0.03
189
Chocolate powder
0.06
0.03
0.08
0.06
190
Gelatin dessert
0.02
T
0.015
191
Soda pop, cola, canned
0.02
0.013
7APPB/E
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PRELIMINARY ORAFT
TABLE 7D-1. (continued)
Category Food Lead concentration* Mean*
(Mfl/fl)
192
Soda pop lemon-line, canned 0.13
0.02
0.02
0.06
193
Soft drink powder
0.02
0.013
194
Soda pop, cola, low cal.,
canned
0.05
0.02
0.027
195
Coffee, instant
0.01
196
Coffee, instant, decaf.
0.02
0.013
197
Tea
0.01
198
Beer, canned
0.02
0.02
0.17
199
Wine
0.03
0.03
0.03
0.03
200
Whiskey
0.02
0.013
201
Water
T
0.012
*Individua1 values for three Market Basket Surveys. "T" means only a trace detected, missing
+value means below detection Unit,
Means determined by EPA using 0.01 (% of detection Unit) for missing values and
0.015 for "T".
7APPB/E
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PRELIMINARY DRAFT
TABLE 7D-2. CONDENSATION, TO 25 CATEGORIES, OF THE
201 CATEGORIES OF FOOD
Table 7-13 Categories and fractional categories*
category fron Pennington (1983) (Table 70-1)
Milk
1-6, 9
Dairy Products
7, 10-12, 164, 167, 174, 176, 177
Milk as ingredient
0.5(156), 0.2(178-187)
Beef
13-16, 0.1(143), 0.3(145), 0.6(147, 0.4(142, 149)
Pork
17-21
Chicken
24-26
F1sh
31-34
Prepared meats
28-30
Other meats
22-23, 27
Eggs
35-37, 0.15(142, 144, 146, 149), 0.2(178-187), 0.3(69, 70)
Bread
58, 59, 61, 62, 65, 68, 0.4(147)
Flour as Ingredient
159, 160, 0.3(142, 144, 146, 149, 178-187), 0.6(69, 70)
Non-wheat cereals
50-52, 64, 75-77
Corn flour
53, 60, 63, 67, 71
Leafy vegetables
107-111, 113-116
Root vegetables
127, 128, 132
Vine vegetables
38, 40-44, 46, 117, 121, 123-126, 161, 173
Canned vegetables
39, 45, 106, 112, 118-120, 122, 129-131, 0.1(142, 145, 149)
0.2(144), 0.5(155-157)
Sweet corn
54
Canned sweet corn
55, 56
Potatoes
134-141
Vegetable oil
162, 163, 165, 166
169-172, 188, 0.3(178-187)
Sugar
Canned fruits
82, 84, 87, 90, 93
78-81, 83, 85, 86, 88, 89, 91, 92, 94-97
Fresh fruits
*In some cases, only a fraction of a category, e.g., milk in tomato soup, was used, and this
fraction 1s Indicated by a decimal fraction before the category number in parenthesis.
7APPB/E
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PRELIMINARY DRAFT
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8. EFFECTS OF LEAD ON ECOSYSTEMS
8.1 INTRODUCTION
8.1.1 Scope of Chapter 8
This chapter describes the potential effects of atmospheric lead inputs on several types
of ecosystems. An effect 1s any condition attributable to lead that causes an abnormal phy-
siological response in individual organisms or that perturbs the normal processes of an eco-
system. A distinction is made among natural, cultivated, and urban ecosystems, and extended
discussions are included on the mobility and bioavailability of lead in ecosystems.
There are many reports on the effects of lead on individual populations of plants and
animals and a few studies on the effects of lead in simulated ecosystems or microcosms.
However, the most realistic studies are those that examine the effects of lead on entire
ecosystems, as they incorporate all of the ecological interactions among the various popu-
lations and all of the chemical and biochemical processes relating to lead (National Academy
of Sciences, 1981). Unfortunately, these studies have also had to cope with the inherent
variability of natural systems and the confounding frustrations of large scale projects.
Consequently, there are only a handful of ecosystem studies on which to base this report.
The principle sources of lead entering an ecosystem are: the atmosphere (from automotive
emissions), paint chips, spent ammunition, the application of fertilizers and pesticides, and
the careless disposal of lead-acid batteries or other industrial products. Atmospheric lead
is deposited on the surfaces of vegetation as well as on ground and water surfaces. In
terrestrial ecosystems, this lead Is transferred to the upper layers of the soil surface,
where it may be retained for a period of several years. The movement of lead within eco-
systems is influenced by the chemical and physical properties of lead and by the biogeo-
chemical properties of the ecosystem. Lead is non-degradable, but in the appropriate chemical
environment, may undergo transformations which affect its solubility (e.g., formation of lead
sulfate in soils), its bioavailability (e.g., chelation with humic substances), or its toxi-
city (e.g., chemical methylation).
The previous Air Quality Criteria for Lead (U.S. Environmental Protection Agency, 1977)
recognized the problems of atmospheric lead exposure incurred by all organisms including man.
Emphasis in the chapter on ecosystem effects was given to reports of toxic effects on specific
groups of organisms, e.g. domestic animals, wildlife, aquatic organisms, and vascular and non-
vascular plants. Forage containing lead at 80 pg/g dry weight was reported to be lethal to
horses, whereas 300 pg/g dry weight caused lethal clinical symptoms in cattle. This report
will attempt to place the data in the context of sublethal effects of lead exposure, to extend
the conclusions to a greater variety of domestic animals, and to describe the types and ranges
of exposures in ecosystems likely to present a problem for domestic animals.
PB8A/B 8-1 7/13/83
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Research on lead in wildlife has traditionally fallen into the following somewhat arti-
ficial categories: waterfowl; birds and small mammals; fish; and invertebrates. In all these
categories, no correlation could be made 1n the 1977 report between toxic effects and environ-
mental concentrations. Some recent toxicity studies have been completed on fish and Inverte-
brates and the data are reported below, but there is still little Information on the levels of
lead that can cause toxic effects in small mammals or birds.
Information on the relationship between soil lead and plants can be expanded somewhat
beyond the 1977 report, primarily due to a better understanding of the role of humic sub-
stances in binding lead. Although the situation is extremely complex, it is reasonable to
state that most plants cannot survive in soil containing 10,000 pg/g dry weight 1f the pH Is
below 4.5 and the organic content is below 5 percent. The specifics of this statement are
discussed more extensively in Section 8.3.1.2.
Before 1977, natural levels of lead in environmental media other than soil were not well
known. Reports of sublethal effects of lead were sparse and there were few studies of total
ecosystem effects. Although several ecosystem studies have been completed since 1977 and many
problems have been overcome, it is still difficult to translate observed effects under speci-
fic conditions directly to predicted effects in ecosystems. Some of the known effects, which
are documented in detail in the appropriate sections, are summarized here:
Plants. The basic effect of lead on plants is to stunt growth.
This may be through a reduction of photosynthetlc rate,
inhibition of respiration, cell elongation, or root deve-
lopment, or premature senescence. Some genetic effects
have been reported. All of these effects have been ob-
served in Isolated cells or in hydroponically-grown plants
in solutions comparable to 1 to 2 pg/g soil moisture.
These concentrations are well above those normally found
in any ecosystem except near smelters or roadsides.
Terrestrial plants take up lead from the soil moisture and
most of this lead is retained by the roots. There is no
evidence for foliar uptake of lead and little evidence
that lead can be translocated freely to the upper portions
of the plant. Soil applications of calcium and phosphorus
may reduce the uptake of lead by roots.
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Animals. Lead affects the central nervous system of animals and
their ability to synthesize red blood cells. Blood con-
centrations above 0.4 ppm (40 jjg/dl) can cause observable
clinical symptoms in domestic animals. Calcium and phos-
phorus can reduce the intestinal absorption of lead. The
physiological effects of lead exposures in laboratory
animals are discussed in extensive detail in Chapters 10
and 12 of this document.
Hicroorganisms.There is evidence that lead at environmental concen-
trations occasionally found near roadsides and smelters
(10,000 to 40,000 pg/g dw) can eliminate populations of
bacteria and fungi on leaf surfaces and in soil. Many of
those micoorganisms play key roles in the decomposition
food chain. It is likely that the affected microbial
populations are replaced by others of the same or differ-
ent species, perhaps less efficient at decomposing organic
matter. There is also evidence that microorganisms can
mobilize lead by making it more soluble and more readily
taken up by plants. This process occurs when bacteria
exude organic acids that lower the pH in the immediate
vicinity of the plant root.
Ecosystems. There are three known conditions under which lead may
perturb ecosystem processes. At soil concentrations of
1,000 Mfl/g oi" higher, delayed decomposition may result
from the elimination of a single population of decomposer
microorganisms. Secondly, at concentrations of 500 to
1,000 |ig/g, populations of plants, microorganisms, and
invertebrates may shift toward lead tolerant populations
of the same or different species. Finally, the normal
biogeochemical process which purifies and repurifies
calcium in grazing and decomposer food chains may be
circumvented by the addition of lead to vegetation and
animal surfaces. This third effect can be measured at all
ambient atmospheric concentrations of lead.
Some additional effects may occur due to the uneven dis-
tribution of lead in ecosystems. It is known that lead
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accumulates in soil, especially soil with high organic
content. Although no firm documentation exists, it is
reasonable to assume from the known chemistry of lead in
soil that: 1) other metals may be displaced from the
binding sites on the organic matter; 2) the chemical
breakdown of inorganic soil fragments may be retarded by
the Interference of lead on the action of fulvic acid on
iron bearing crystals; and 3) lead in soil may be in
equilibrium with moisture films.surrounding soil particles
and thus available for uptake by plants.
To aid the reader in understanding the effects of lead on ecosystems, sections have been
included that discuss such important matters as how ecosystems are organized, what processes
regulate metal cycles, what criteria are valid in interpreting ecosystem effects, and how soil
systems function to regulate the controlled release of nutrients to plants. The informed
reader may wish to turn directly to Section 8.3, where the discussion of the effects of lead
on organisms begins.
8.1.2 Ecosystem Functions
8.1.2.1 Types of Ecosystems. Based on ambient ciiKfcentrat'ions of atmospheric lead and the dis-
tribution of lead in the soil profile, it is useful to distinguish among three types of eco-
systems: natural, cultivated, and urban. Natural ecosystems include aquatic and terrestrial
ecosystems that are otherwise unperturbed by man, and those managed ecosystems, such as com-
mercial forests, grazing areas, and abandoned fields, where the soil profile has remained un-
disturbed for several decades. Cultivated ecosystems include those where the soil profile is
frequently disturbed and those where chemical fertilizers, weed killers, and pest-control
agents may be added. In urban ecosystems, a significant part of the exposed surface includes
rooftops, roadways, and parking lots from which runoff, if not channeled into municipal waste
processing plants, is spread over relatively small areas of soil surface. The ambient air
concentration of lead in urban ecosystems is 5 to 10 times higher than in natural or culti-
vated ecosystems (See Chapter 7). Urban ecosystems may also be exposed to lead from other
than atmospheric sources, such as paint, discarded batteries, and used motor oil. The effects
of atmospheric lead depend on the type of ecosystems examined.
8.1.2.2 Energy Flow and Biogeochemical Cycles. Two principles govern ecosystem functions:
1) energy flows through an ecosystem; and 2) nutrients cycle within an ecosystem. Energy
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usually enters the ecosystem in the form of sunlight and leaves as heat of respiration.
Stored chemical energy nay be transported into or out of an ecosystem (e.g., leaf detritus in
a stream) or be retained by the ecosystem for long periods of time (e.g., tree trunks).
Energy flow through an ecosystem nay give structure to the ecosystem by establishing food webs
which efficiently regulate the transfer of energy. Segments of these food webs are called
food chains. Energy that flows along a grazing food chain is diverted at each step to the
detrital food chain. ;
Unlike energy, nutrient and non-nutrient elements are recycled by the ecosystem and
transferred from reservoir to reservoir in a pattern usually referred to as a biogeochemical
cycle (Brewer, 1979, p. 139). The reservoirs correspond approximately to the food webs of
energy flow. Although elements may enter (e.g., weathering of soil) or leave the ecosystem
(e.g., stream runoff), the greater fraction of the available mass of the element is usually
cycled within the ecosystem.
Two important characteristics of a reservoir are the amount of the element that may be
stored in the reservoir and the rate at which the element enters or leaves the reservoir.
Some reservoirs may contain a disproportionately large amount of a given element. For exam-
ple, most of the carbon in a forest is bound in the trunks and roots of trees, whereas most of
the calcium may be found in the soil (Smith, 1980, p. 316). Some large storage reservoirs,
such as soil, are not actively involved in the rapid exchange of the nutrient element, but
serve as a reserve source of the element through the slow exchange with a more active reser-
voir, such as soil moisture. When inputs exceed outputs, the size of the reservoir increases.
Increases of a single element may reflect instability of the ecosystem. If several elements
increase simultaneously, this expansion may reflect stable growth of the community.
Reservoirs are connected by pathways which represent real ecosystem processes. Figure
8-1 depicts the biogeochemical reservoirs and pathways of a typical terrestrial ecosystem.
Most elements, especially those with no gaseous phase, do not undergo changes in oxidation
state and are equally available for exchange between any two reservoirs, provided a pathway
exists between the two reservoirs. The chemical environment of the reservoir may, however,
regulate the availability of an element by controlling solubility or binding strengths. This
condition is especially true for soils.
Ecosystems have boundaries. These boundaries may be as distinct as the border of a pond
or as arbitrary as an imaginary circle drawn on a map. Many trace metal studies are conducted
in watersheds where some of the boundaries are determined by topography. For atmospheric
inputs to terrestrial ecosystems, the boundary is usually defined as the surface of vegeta-
tion, exposed rock, or soil. The water surface suffices for aquatic ecosystems.
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GRAZERS
HERBIVORES
CARNIVORES
CARNIVORES
PRIMARY
PRODUCERS
DECOMPOSERS
DETRITUS
INORGANIC
NUTRIENTS
Figure 8-1. This figure depicts cycling processes within the major components of a
terrestrial ecosystem, i.e. primary producers, grazers and decomposers. Nutrient and
non-nutrient elements are stored in reservoirs within these components. Processes
that take place within reservoirs regulate the flow of elements between reservoirs
along established pathways. The rate of flow Is In part a function of the concentra-
tion in the preceding reservoir. Lead accumulates in decomposer reservoirs which
have a high binding capacity for this metal. It Is likely that the rate of flow away
from these reservoirs has increased in past decades and will continue to Increase for
some time until the decomposer reservoirs are in equilibrium with the entire
ecosystem. Inputs to and outputs from the ecosystem as a whole are not shown.
Source: Adapted from Swift et al. (1979).
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Non-nutrient elements differ little from nutrient elements in their biogeochemical cy-
cles. Quite often, the cycling patterns are similar to those of a major nutrient. In the
case of lead, the reservoirs and pathways are very similar to those of calcium.
The important questions are: Does atmospheric lead interfere with the normal mechanisms
of nutrient cycles? How does atmospheric lead influence the normal lead cycle in an eco-
system? Can atmospheric lead interfere with the normal flow of energy through an ecosystem?
8.1.2.3 Biogeochemistry of Lead. Naturally occurring lead from the earth's crust is coamonly
found in soils and the atmosphere. Lead may enter an ecosystem by weathering of parent rock
or by deposition of atmospheric particles. This lead becomes a part of the nutrient medium of
plants and the diet of animals. All ecosystems receive lead from the atmosphere. More than
99 percent of the current atmospheric lead deposition is now due to human activities (National
Academy of Sciences, 1980). In addition, lead shot from ammunition may be found in many
waterways and popular hunting regions, leaded paint chips often occur in older urban regions
and lead in fertilizer may contaminate the soil in agricultured regions.
In prehistoric times, the contribution of lead from weathering of soil was probably about
4 g Pb/ha-yr and from atmospheric deposition about 0.02 g Pb/ha*yr, based on estimates of
natural and anthropogenic emissions in Chapter 5 and deposition rates discussed in Chapter 6.
Weathering rates are presumed to have remained the same, but atmospheric inputs are believed
to have increased to 180 g/ha*yr in natural and some cultivated ecosystems, and 3,000 g/ha*yr
in urban ecosystems and along roadways (see Chapter 6). In every terrestrial ecosystem of the
Northern Hemisphere, atmospheric lead deposition now exceeds weathering by a factor of at
least 10, sometimes by as much as 1,000.
Many of the effects of lead on plants, microorganisms, and ecosystems arise from the fact
that lead from atmospheric and weathering inputs is retained by soil. Geochemlcal studies
show that less than 3 percent of the inputs to a watershed leave by stream runoff (Siccama and
Smith, 1978; Shirahata et al,, 1980). In prehistoric times, stream output nearly equalled
weathering inputs and the lead content of soil probably remained stable, accumulating at an
annual rate of less than 0.1 percent of the original natural lead (reviewed by Nriagu, 1978).
Due to human activity, lead in natural soils now accumulates on the surface at an annual rate
of 5 to 10 percent of the natural lead. One effect of cultivation is that atmospheric lead is
mixed to a greater depth than the 0 to 3 cm of natural soils.
Most of the effects on grazing vertebrates stem from the deposition of atmospheric parti-
cles on vegetation surfaces. Atmospheric deposition may occur by either of two mechanisms.
Wet deposition (precipitation scavenging through rainout or washout) generally transfers lead
directly to the soil. Dry deposition transfers particles to all exposed surfaces, large
particles (>4 af"e transferred by gravitational mechanisms, small particles (<0.5 |jm) are
also deposited by wind-related mechanisms.
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About half of the foliar dry deposition remains on leaf surfaces following normal rain-
fall (Elias et al., 1976; Peterson, 1978), but heavy rainfall isay transfer the lead to other
portions of the plant (Elias and Croxdale, 1980). Koeppe (1981) has reviewed the literature
and concluded that less than 1 percent of the surface lead can pass directly into the internal
leaf tissues of higher plants. The cuticular layer of the leaves is an effective barrier to
aerosol particles and even to metals in solution on the leaf surface (Arvik and Zimdahl,
1974), and passage through the stomata cannot account for a significant fraction of the lead
inside 1 eaves (Carlson et al., 1976; 1977).
When particles attach to vegetation surfaces, transfer to soil is delayed from a few
months to several years. Due to this delay, large amounts of lead are diverted to grazing
food chains, bypassing the soil moisture and plant root reservoirs (Elias et al., 1982).
8.1.3 Criteria for Evaluating Ecosystem Effects
As it is the purpose of this chapter to describe the levels of atmospheric lead that nay
produce adverse effects in plants, animals, and ecosystens, it is necessary to establish the
criteria for evaluating these effects. The first step is to determine the connection between
air concentration and ecosystem exposure. If the air concentration is known, ecosystem inputs
fron the atmosphere can be predicted over tine and under normal conditions. These inputs and
those from the weathering of soil determine the concentration of lead in the nutrient Media of
plants, animals, and microorganisms. It follows that the concentration of lead in the nutri-
ent medium determines the concentration of lead in the organism and this in turn determines
the effects of lead on the organism.
The fundamental nutrient medium of a terrestrial ecosystem is the soil moisture film
which surrounds organic and inorganic soil particles. This film of water is in equilibrium
with other soil components and provides dissolved inorganic nutrients to plants. It is chemi-
cally different than ground water or rain water and there is little reliable information on
the relationship between lead in soil and lead in soil moisture. Thus, it appears impossible
to quantify all the steps by which atmospheric lead is transferred to plants. Until more
information is available on lead in soil moisture, another approach m«y be more productive.
This involves determining the degree of contamination of organisms by comparing the present
known concentrations with calculated prehistoric concentrations.
Prehistoric concentrations of lead have been calculated for only a few types of organ-
Isms. However, the results are so low that any normal variation, even of an order of magni-
tude, would not seriously alter the degree of contamination. The link between lead 1n the
prehistoric atmosphere and in prehistoric organisms may allow us to predict concentrations of
lead in organisms based on present or future concentrations of atmospheric lead.
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It is reasonable to infer a relationship between degree of contain nation and physio-
logical effect. It seems appropriate to assume that natural levels of lead which were safe
for organisms in prehistoric times would also be safe today. It is also reasonable that sone
additional atmospheric lead can be tolerated by all populations of organisms with no ill
effects, that some populations are more tolerant than others, and that some individuals within
populations are more tolerant of lead effects than others.
For nutrient elements, the concept of tolerance is not new. The Law of Tolerance
(illustrated in Figure 8-2) states that any nutrient may be present at concentrations either
too low or too high for a given population and that the ecological success of a population is
greatest at some optimum concentration of the nutrient (Smith, 1980, p. 35). In a similar
manner, the principle applies to non-nutrient elements. Although there is no minimum concen-
tration below which the population cannot survive, there is a concentration above which the
success of the population will decline (point of Initial response) and a concentration at
which the entire population will die (point of absolute toxicity). In this respect, both
nutrients and non-nutrients behave in a similar manner at concentrations above some optimum.
Certain variables make the points of initial response and absolute toxicity somewhat
Imprecise. The point of initial response depends on the type of response investigated. This
response may be at the molecular, tissue, or organismic level, with the molecular response
occurring at the lowest concentration. Similarly, at the point of absolute toxicity, death
may occur instantly at high concentrations or over a prolonged period of time at somewhat
lower concentrations. Nevertheless, the gradient between these two points remains an appro-
priate basis on which to evaluate known environmental effects, and any information which
correctly positions this part of the tolerance curve will be of great value.
The normal parameters of a tolerance curve, i.e., concentration and ecological success,
can be replaced by degree of contamination and percent physiological dysfunction, respectively
(Figure 8-3). Use of this method of expressing degree of contamination should not imply that
natural levels are the only safe levels. It is likely that some degree of contamination can
be tolerated with no physiological effect.
Data reported by the National Academy of Sciences (1980) are used to determine the typi-
cal natural lead concentrations shown in various compartments of ecosystems in Table 8-1.
These data are from a variety of sources and are simplified to the most probable value within
the range reported by NAS. The actual prehistoric air concentration was probably near the low
end of the range (0.02-1.0 ng/m3), as present atmospheric concentrations of 0.3 ng/m4 in the
Southern Hemisphere and 0.07 ng/m3 at the South Pole (Chapter 5), would seem to preclude natu-
ral lead values higher than this.
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NON-NUTRIENT
MAXIMUM
I NUTRIENT
ui
ABSOLUTS
TOXICITY
LOW
HIGH
CONCENTRATION OF ELEMENT
Figure M. The ecological euccess of • population depends in part on the availability
of all nutrients at aoma optimum concentration. The dashed Una of this diagram
da plots tha rlaa and decline of ecological success (the ability of a population to grow,
survive ami raproduca) ovar a wide concentration range of a single alament Tha
curve need not bo symmetrically beli-shaped, but may be skewed to ttw right or left
Although the range in concentration that permits maximum success may be much
wider than shown here, tha Important point ia that at aoma high concantratlon, tha
nutrient element becomes toxic. The tolerance of populations for high concentrations
of non-nutrients (solid Una) la similar to that of nutrients, although than ia not yet
any scientific basis for deacrlbing tha exact shape of this portion of the curve.
Source: Adapted from Smith (19801.
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MHTMUIY ZONE Of AMUMEO
*AFE CONCENTRATION
| 1
NATURAL
CONCENTRATION
T-
mrrm. s,
RESPONSE N 4
I
i
OBSERVED N .
OY8FUNCTKM
- DEOREE OF CONTAMINATION -
nn AMOLim
s
w
1006
IftfiOO
OWCftVEO COftIC./NATURAL CONC.
Component
Rgura »-3. TM* ftgur* attampta to reconstruct the right portion of ¦ tolaranca curva. tlmllar to
Hgura 8-2 but ptottsd on a m ml log tcala. for a population udng • Imltod amount of information.
H tha natural eoneantratlon ia known for a population and »It ia arbitrarily aaaumad that lOx
natural concantratfon if also tafa, than tha zona of auumad aafa eoneantratlon daflnaa tha
raglon.
TABLE 8-1. ESTIMATED NATURAL LEVELS OF LEAD IN ECOSYSTEMS
Best estimate
Range
Air
0.01-1.0 ng/m3
0.07
Soil
Inorganic
5-25 pg/g
12.0
Organic
1 Nfl/fl
1.0
Soil moisture
0.0002 Mg/g
0.0002
Plant leaves
o.oi-o.i pg/g dw
0.05
Herbivore bones
0.04-0.12 jjg/g dw
0.12
Carnivore bones
0.01-0.03 jjg/g dw
0.03
Source: Ranges are from the National Academy of Sciences,(1980j;best estimates are discussed
in the text. Units for best estimates are the same as for ranges.
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In prehistoric times, the rate of entry of lead into the nutrient pool available to
plants was predominantly determined by the rate of weathering of inorganic minerals in frag-
ments of parent rock material. Geochenical estimates of denudation and adsorption rates
(Chapter 6) suggest a median value of 12 pg/g as the average natural lead content of total
soil, with the concentration in the organic fraction at approximately 1 pg/g.
Studies have shown the lead content of leafy vegetation to be 90 percent anthropogenic,
even in remote areas (Crump and Barlow, 1980; Elias et al., 1976, 1978). The natural lead
content of nuts and fruits m*y be somewhat higher than leafy vegetation, based on internal
lead concentrations of modem samples (Elias et al., 1982). The natural lead concentrations
of herbivore and carnivore bones were reported by Elias et al. (Elias and Patterson, 1980;
Elias et al., 1982). These estimates are based on predicted Pb/Ca ratios calculated from the
observed biopurification of calcium reservoirs with respect to Sr, 8a, and Pb, on the system-
atic evaluation of anthropogenic lead inputs to the food chain (Section 8.5.3), and on
measurements of prehistoric mammalian bones.
8.2 LEAD IN SOILS AND SEDIMENTS
2.1 Distribution of Lead in Soils
Because lead in soil is the source of most effects on plants, microorganisms, and eco-
systems, it is important to understand the processes that control the accumulation of lead in
soil. The major components of soil are: 1) fragments of inorganic parent rock material;
2) secondary inorganic minerals; 3) organic constituents, primarily humic substances, which
are residues of decomposition or products of decomposer organisms; 4) Fe-Mn oxide films, which
coat the surfaces of all soil particles and appear to have a high binding capacity for metals;
5) soil microorganisms, most commonly bacteria and fungi, although protozoa and soil algae may
also be found; and 6) soil moisture, the thin film of water surrounding soil particles which
is the nutrient medium of plants. Some watershed studies consider that fragments of inorganic
parent rock material lie outside the forest ecosystem, because transfer from this compartment
is so slow that much of the material remains inert for centuries.
The concentration of lead ranges from 5 to 30 pg/g in the top 5 cm of most soils not
adjacent to sources of industrial lead, although 5 percent of the soils contain as much as
800 pg/g (Chapter 5). Aside from surface deposition of atmospheric particles, plants in North
America average about 0.5 to 1 pg/g dw (Peterson, 1978) and animals roughly 2 pg/g (Forbes and
Sanderson, 1978). Thus, soils contain the greater part of total ecosystem lead. In soils,
lead in parent rock fragments is tightly bound within the crystalline structures of the
Inorganic soil minerals. It is released to the ecosystem only by surface contact with soil
moisture films.
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Hutchinson (1980) has reviewed the effects of acid precipitation on the ability of soils
to retain cations. Excess calcium and other metals are leached fro# the A horizon of soils by
rain with a pH more acidic than 4.5. Most soils in the eastern United States are normally
acidic (pH 3.5 to 5.2) and the leaching process is a part of the complex equilibrium main-
tained in the soil system. By increasing the leaching rate, acid rain can reduce the availa-
bility of nutrient metals to organisms dependent on the top layer of soil. Tyler (1978)
reports the effect of acid rain on the leaching rate (reported as residence time) for lead and
other metals. Simulated rain of pH 4.2 to 2.8 showed the leaching rate for lead increases
with decreasing pH, but not nearly as much as that of other metals, especially Cu, Mn, and Zn.
This would be as expected from the high stability constant of lead relative to other metals in
humic acids (see Section 6.5.1). It appears from this limited information that acidification
of soil may increase the rate of removal of lead from the soil, but not before several major
nutrients are removed first. The effect of acid rain on the retention of lead by soil mois-
ture is not known.
8.2.2 Origin and Availability of Lead in Aquatic Sediments
Atmospheric lead may enter aquatic ecosystems by wet or dry deposition (Dolske and
Sievering, 1979) or by the erosional transport of soil particles (Baier and Healy, 1977). In
waters not polluted by industrial, agricultural, or municipal effluents, the lead concentra-
tion is usually less than 1 jjg/1. Of this amount, approximately 0.02 ijg/1 is natural lead and
the rest is anthropogenic lead, probably of atmospheric origin (Patterson, 1980). Surface
waters mixed with urban effluents may frequently reach lead concentrations of 50 jjg/1, and
occasionally higher (Bradford, 1977).
In aqueous solution, virtually all lead 1s divalent, as tetravalent lead can exist only
under extremely oxidizing conditions (reviewed by Rickard and Nriagu, 1978; Chapter 3). At pH
higher than 5, divalent lead can form a number of hydroxyl complexes, most commonly PbOH+,
Pb(0H)2, and Pb(0H)3 . At pH lower than 5, lead exists in solution as hydrated Pb. In still
water, lead 1s removed from the water column by the settling of lead-containing particulate
matter, by the formation of insoluble complexes, or by the adsorption of lead onto suspended
organic particles. The rate of sedimentation is determined by temperature, pH, oxidation-
reduction potential, ionic competition, the chemical form of lead in water, and certain bio-
logical activities (Jenne and Luoma, 1977). McNurney et al. (1977) found 14 ^9 Pb/fl 1n stream
sediments draining cultivated areas and 400 yg/g in sediments associated with urban eco-
systems. Small sediment grain size and high organic content contributed to increased reten-
tion 1n sediments.
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8.3 EFFECTS OF LEAD ON PLANTS
8.3.1 Effects on Vascular Plants and Algae
Some physiological and biochemical effects of lead on vascular plants have been detected
under laboratory conditions at concentrations higher than normally found in the environment.
The commonly reported effects are the inhibition of photosynthesis, respiration or cell
elongation, all of which reduce the growth of the plant (Koeppe, 1981). Lead may also induce
premature senescence, which may affect the long-term survival of the plant or the ecological
success of the plant population. To provide a meaningful evaluation of these effects, it is
necessary to examine the correlation between laboratory conditions and typical conditions in
nature with respect to form, concentration, and availability of lead. First, the reader must
understand what is known of the movement of lead from soil to the root to the stem and finally
to the leaf or flower. Most notably, there are specific barriers to lead at the soi 1: soi 1
moisture interface and at the root:shoot interface which retard the movement of lead and
reduce the impact of lead on photosynthetic and meristematic (growth and reproduction) tissue.
8.3.1.1 Uptake by Plants. Most of the lead in or on a plant occurs on the surfaces of leaves
and the trunk or stem. The surface concentration of lead in trees, shrubs, and grasses
exceeds the internal concentration by a factor of at least five (Elias et al, 1978). There is
little or no evidence of lead uptake through leaves or bark. Foliar uptake, if it does occur,
cannot account for more than 1 percent of the uptake by roots, and passage of lead through
bark tissue has not been detected (Arvik and Zimdahl, 1974; reviewed by Koeppe, 1981; Zindahl,
1976). Krause and Kaiser (1977) were able to show foliar uptake and translocation of lead
mixed with cadmium, copper, and manganese oxides when applied in large amounts (122 mg/a2)
directly to leaves. This would be comparable to 100,000 days accumulation at a remote site
(0.12 ng/cm*-d) (Elias et al., 1978). The uptake of lead was less than that of other metals
and application of sulfur dioxide did not increase the foilar uptake of these metals. The
major effect of surface lead at ambient concentrations seems to be on subsequent components of
the grazing food chain (Section 8.4.1) and on the decomposer food chain following litterfall
(Elias et al., 1982). (See also Section 8.4.2.)
Uptake by roots is the only major pathway for lead into plants. The amount of lead that
enters plants by this route is determined by the availability of lead in soil, with apparent
variations according to plant species. Soil cation exchange capacity, a major factor, is
determined by the relative size of the clay and organic fractions, soil pH, and the amount of
Fe-Mn oxide films present (Nriagu, 1978). Of these, organic humus and high soil pH are the
dominant factors in immobilizing lead (Chapter 6). Under natural conditions, most of the
total lead in soil would be tightly bound within the crystalline structure of inorganic soil
fragments, unavailable to soi 1 moisture. Available lead, bound on clays, organic colloids,
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and Fe-Mn films, would be controlled by the slow release of bound lead from inorganic rock
sources. Since before 3000 B.C., atmospheric lead inputs through litter decomposition have
increased the pool of available lead bound on organic matter within the soil reservoir (see
Section 5.1).
Because lead is strongly immobilized by humic substances, only a small fraction (perhaps
0.01 percent in soils with 20 percent organic matter, pH 5.5) is released to soil moisture
(see Chapter 6). In soil moisture, lead may pass along the pathway of water and nutrient
uptake on either a cellular route through the cell membranes of root hairs (symplastic route)
or an extracellular route between epidermal cells into the intercellular spaces of the root
cortex (apoplastic route) (Foy et al., 1978). Lead probably passes into the symplast by mem-
brane transport mechanisms similar to the uptake of calcium or other bivalent cations.
At 500 pg Pb/g nutrient solution, lead has been shown to accumulate in the cell walls of
germinating Raphinus sativus roots (Lane and Martin, 1982). This concentration is much higher
than that found by Wong and Bradshaw (1982) to cause inhibition of germinating root elongation
(less than 2.5 pg/g), absence of root growth (5 pg/g), or 55 percent inhibition of seed ger-
mination (20 to 40 MSf/g) in the rye grass, Colium perenne. Lane and Martin (1982) also
observed lead in cytoplasmic organelles which appeared to have a storage function because of
their osmiophillic properties. It was suggested that the organelles eventually emptied their
contents into the tonoplast.
The accumulation of lead in cell walls and cytoplasmic bodies has also been observed in
blue green algae by Jensen et al. (1982), who used X-ray energy dispersive analysis in con-
junction with scanning electron microscopy to observe high concentrations of lead and other
metals in these single celled procaryotic organisms. They found the lead concentrated in the
third of the four layered cell wall and in polyphosphate bodies (not organelles, since they
are not membrane-bound) which appeared to be a storage site for essential metals. The nutri-
ent solution contained 100 m9 Pb/g- The same group (Rachlin et al., 1982) reported morpholo-
gical changes in the same blue green alga (Plectonema boryanum). There was a significant
increase In cell size caused by the lead, which indicated that the cell was able to detoxify
its cytoplasm by excreting lead with innocuous cell wall material.
It appears that two defensive mechanisms may exist in the roots of plants for removing
lead from the stream of nutrients flowing to the above ground portions of plants, lead may be
deposited with cell wall material exterior to the individual root cells, or may be sequestered
in organelles within the root cells. Any lead not captured by these mechanisms would likely
move with nutrient metals cell-to-cell through the symplast and into the vascular system.
Uptake of lead by plants may be enhanced by symbiotic associations with mycorrhizal fungi
The three primary factors that control the uptake of nutrients by plants are the surface area
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of the roots, the ability of the root to absorb particular ions, and the transfer of ions
through the soil. The symbiotic relationship between mycorrhizal fungi and the roots of
higher plants can increase the uptake of nutrients by enhancing all three of these factors
(Voigt, 1969). The typical ectomycorrhiza consists of a mantle or sheath of mycelia that com-
pletely surrounds the root. The physical extension of the sheath nay Increase the volume of
the root two to three tines (Voigt, 1969). Mycorrhizal roots often show greater affinities
for nutrients than do uninfected roots of the sane species grown in the same conditions. In
many soil systems, where the bulk of the nutrients are bound up in parent rock material, effi-
cient uptake of these nutrients by plants depends on the ability of organises in the rhizo-
sphere (plant roots, soil fungi, and bacteria) to increase the rates of weathering. Mycorrhi-
zal fungi are known to produce and secrete into their environment many different acidic com-
pounds (e.g., aalic and oxalic acids). In addition, mycorrhizal roots have been shown to
release more carbon dioxide into the rhizosphere than do non-mycorrhizal roots as a result of
their increased rates of respiration. Carbon dioxide readily combines with soil moisture to
produce carbonic acid. All of these acids are capable of increasing the weathering rates of
soil particles such as clays, and altering the binding capacity of organic material, thereby
increasing the amount of nutrients in the soil solution. Mycorrhizae are known to enhance the
uptake of zinc by pine roots (Bowen et al., X974), and it is likely that lead uptake is simi-
larly increased, by inference to the ability of mycorrhizae to enhance the uptake of calcium
by pine roots (Mel in and Nilsson, 1955; Mel in et al., 1958).
The translocation of lead to aboveground portions of the plant is not clearly understood.
Lead may follow the same pathway and be subject to the same controls as a nutrient metal such
as calcium. This assumption implies that the plant root has no means of discriminating
against lead during the uptake process, and it is not known that any such discrimination
mechanism exists. There may be several mechanisms, however, that excrete lead back out of the
root or that prevent its translocation to other plant parts. The primary mechanisms may be
storage in cell organelles or adsorption on cell walls. The apoplast contains an Important
supply of plant nutrients, including water. Lead in the apoplast remains external to the
cells and cannot pass to vascular tissue without at least passing through the cell membranes
of the endodermis. Because this extracellular region is bounded on all sides by cell walls,
the surface of which Is composed of layers of cellulose strands, the surface area of the
apoplast is comparable to a sponge. It is likely that much of the lead in roots is adsorbed
to the apoplast surface. Oictyosomes, cytoplasmic organelles which contain cell wall
material, may carry lead from inside the cell through the membrane to become a part of the
external cell wall (Malone et al., 1974), possibly replacing calcium in calcium pectate. Lead
may also be stored and excreted as lead phosphate in dictyosome vesicles (Malone et al.,
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1974). Nevertheless, some lead does pass into the vascular tissue, along with water and
dissolved nutrients, and is carried to physiologically active tissue of the plant.
Evidence that lead in contaminated soils can enter the vascular system of plants and be
transported to aboveground parts may be found in the analysis of tree rings. Rolfe (1974)
found four-fold increases in both rural and urban trees using 10 year increments of annual
rings for the period 1910-20 and comparing these to annual rings of the period 1963-73.
Symeonides (1979) found a two-fold increase from 1907-17 to 1967-77 in trees at a high-lead
site, with no increase in trees from a low-lead site. Finally, Baes and Ragsdale (1981),
using only ring porous species, found significant post-1930 increases in Quercus and Carya
with high lead exposure, but only in Carya with low lead exposure. These chronological
records confirm that lead can be translocated from roots to the upper portions of the plant
and that the amounts translocated are in proportion to the concentrations of lead in soil.
8.3.1.2 Physiological Effects on Plants. Because most of the physiologically active tissue of
plants is involved in growth, maintenance, and photosynthesis, it is expected that lead might
interfere with one or more of these processes. Indeed, such interferences have been observed
in laboratory experiments at lead concentrations greater than those normally found in the
field, except near smelters or mines (Koeppe, 1981). It is likely that more is known of these
effects because these are the physiological processes studied more vigorously than others.
Studies of other plant processes, especially maintenance, flowering, and hormone development,
have not been conducted and no conclusion can be reached concerning possible lead effects on
these processes.
Inhibition of photosynthesis by lead may be by direct interference with the light reac-
tion or the indirect interference with carbohydrate synthesis. At 21 pg Pb/g reaction solu-
tion, Miles et al. (1972) demonstrated substantial inhibition of photosystem II near the site
of water splitting, a biochemical process believed to require manganese. Homer et al. (1979)
found a second effect on photosystem II at slightly higher concentrations of lead. This
effect was similar to that of DOW [3-(3,4-dichlorophenyl)-l,l-dimethylurea], a reagent com-
monly used to uncouple the photosynthetic electron transport system. Bazzaz and Govindjee
(1974) suggested that the mechanism of lead inhibition was a change in the conformation of the
thylakoid membranes, separating and isolating pigment systems I and II. Wong and Govindjee
(1976) found that lead also interferes with P700 photooxidation and re-reduction, a part of
the photosystem I light reaction. Homer et al. (1981) found a lead tolerant population of the
grass Phalaris arundinacea had lowered the ratio of chlorophyll a/chlorophyll b, believed to
be a compensation for photosystem II inhibition. There was no change in the total amount of
chlorophyll, but the mechanism of inhibition was considered different than that of Miles et
al. (1972). Hampp and Lendzian (1974) found that lead chloride inhibits the synthesis of
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chlorophyll b more than that of chlorophyll a at concentrations up to 100 mg Pb/g. Devi
Prasad and Devi Prasad (1982) found 10 percent inhibition of pigment production in three spe-
cies of green algae at 1 pg/g, increasing to 50 percent inhibition at 3 pg/g. Bazzaz et al.
(1974, 1975) observed reduced net photosynthesis which may have been caused Indirectly by
inhibition of carbohydrate synthesis. Without carbohydrates, stomatal guard cells remain
flaccid, transpiration ceases, carbon dioxide fixation decreases, and further carbohydrate
synthesis is inhibited.
The stunting of plant growth may be by the inhibition of the growth hormone IAA (indole-
3-ylacetic acid). Lane et al. (1978) found a 25 percent reduction in elongation at 10 pg/g
lead as lead nitrate in the nutrient medium of wheat coleoptiles. This effect could be re-
versed with the addition of calcium at 18 jjg/g. Lead may also interfere with plant growth by
reducing respiration or inhibiting cell division. Miller and Koeppe (1970) and Miller et al.
(1975) showed succinate oxidation inhibition in isolated mitochondria as well as stimulation
of exogenous NADH oxidation with related mitochondrial swelling. Hassett et al. (1976),
Koeppe (1977), and Malone et al. (1978) described significant Inhibition of lateral root
initiation in corn. Inhibition increased with the simultaneous addition of cadmium.
Sung and Yang (1979) found that lead at 1 pg/g can complex with and inactivate ATPase to
reduce the production and utilization of ATP in kidney bean (Phaseolus vulgaris) and buckwheat
leaves (Fagopyrum esculentua). The lead was added hydroponically at concentrations up to
1,000 pg/g. Kidney bean ATPase showed a continued response from 1 to 1,000 pg/g, but buck-
wheat leaves showed little further reduction after 10 pg/g. Neither extracted ATP nor chemi-
cally added ATP could be used by the treated plants. Lee et al. (1976) found a 50 percent
increase in the activity of several enzymes related to the onset of senescence in soybean
leaves when lead was added hydroponically at 20 pg/g. These enzymes were acid phosphatase,
peroxidase, and alpha-amylase. A build-up of ammonia was observed along with a reduction in
nitrate, calcium, and phosphorus. Glutamlne synthetase activity was also reduced by 65 per-
cent. Continued increases in effects were observed up to 100 pg/g, including a build-up of
soluble protein. Piivfike (1979) also observed a 60 percent increase in acid phosphatase acti-
vity during the first 6 days of pea seedling germination (Pisum sativum) at 2 pg/g, under low
nutrient conditions. The accumulation of soluble protein was observed and the effect could be
reversed with the addition of nutrients, including calcium.
The interaction of lead with calcium has been shown by several authors, most recently by
Garland and Wilkins (1981), who demonstrated that barley seedlings (Hordeum vulgare). which
were growth inhibited at 2 pg Pb/g sol. with no added calcium, grew at about half the control
rate with 17 pg Ca/g sol. This relation persisted up to 25 pg Pb/g sol. and 500 pg Ca/g sol.
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These studies of the physiological effects of lead on plants all show some effect at
concentrations from 2 to 10 |jg/g in the nutrient medium of hydroponically-grown agricultural
plants. It is certain that no effects would have been observed at these concentrations had
the lead solutions been added to normal soil, where the lead would have been bound by humic
substances. There is no firm relationship between soil lead and soil moisture lead, because
each soil type has a unique capacity to retain lead and to release that lead to the soil
moisture film surrounding the soil particle. Once in soil moisture, lead seems to pass freely
to the plant root according to the capacity of the plant root to absorb water and dissolved
substances (Koeppe, 1981).
Chapter 6 discusses the many parameters controlling the release of lead from soil to soil
moisture, but so few data are available on observed lead concentrations in soil moisture that
no model can be formed. It seems reasonable that there may be a direct correlation between
lead in hydroponic media and lead in soil moisture. Hydroponic media typically have an excess
of essential nutrients, including calcium and phosphorus, so that movement of lead from hydro-
ponic media to plant root would be equal to or slower than movement from soil moisture to
plant root. Hughes (1981) adopted the general conclusion that extractable soil lead is typi-
cally 10 percent of total soil lead. However, this lead was extracted chemically under lab-
oratory conditions more rigorous than the natural equilibrium between soil and soil moisture.
Ten percent should therefore be considered the upper limit, where the ability of soil to
retain lead is at a minimum. A lower limit of 0.01 percent is based on the only known report
of lead in both soil and soil moisture (16 pg/g soil, 1.4 pg/g soil moisture; Elias et al. ,
1982). This single value shows neither trends with different soil concentrations nor the soil
component (organic or inorganic) that provides the lead to the soil moisture. But the number
(0.01 percent) is a conservative estimate of the ability of soil to retain lead, since the
conditions (pH, organic content) were optimum for retaining lead. A further complication is
that atmospheric lead is retained at the surface (0-2 cm) of the soil profile (Martin and
Coughtrey, 1981), whereas most reports of lead in soil pertain to samples from 0 to 10 cm as
the "upper" layer of soil. Any plant that absorbs solely from the top few centimeters of soil
obviously is exposed to more lead than one with roots penetrating to a depth of 25 cm or more.
Agricultural practices that cultivate soil to a depth of 25 cm blend in the upper layers with
lower to create a soil with average lead content somewhat above background.
These observations lead to the general conclusion that even under the best of conditions
where soil has the highest capacity to retain lead, most plants would experience reduced
growth rate (inhibition of photosynthesis, respiration, or cell elongation) in soils of 10,000
MO Pb/g or greater. Concentrations approaching this value typically occur around smelters
(Martin and Coughtrey, 1981) and near major highways (Wheeler and Rolfe, 1979). These con-
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elusions pertain to soil with the ideal composition and pH to retain the maximum amount of
lead. Acid soils or soils lacking organic matter would inhibit plants at much lower lead
concentrations.
The rate at which atmospheric lead accumulates in soil varies from 1.1 mg/m2»yr average
global deposition (Table 6-7) to 3,000 mg/m2*yr near a smelter (Patterson et al., 1975).
Assuming an average density of 1.5 g/cm3, undisturbed soil to a depth of 2 cm (20,000 cm3/ra2)
would Incur an Increase in lead concentration at a rate of 0.04 to 100 pg/g soil-yr. This
means remote or rural area soils may never reach the 10,000 pg/g threshold but that undis-
turbed soils closer to major sources may be within range in the next 50 years.
8.3.1.3 Lead Tolerance in Vascular Plants. Some plant species have developed populations
tolerant to high lead soils (Antonovics et al., 1971). In addition to Homer et al. (1981)
cited above, Jowett (1964) found populations of Agrostls tenuis in pure stands on acidic spoil
banks near an abandoned mine. The exclusion of other species was attributed to root inhibi-
tion. Populations of A. tenuis from low-lead soils had no tolerance for the high lead soils.
Several other studies suggest that similar responses may occur in populations growing in
lead-rich soils (reviewed in Peterson, 1978). A few have suggested that crops may be culti-
vated for their resistance to high lead soils (Gerakis et al., 1980; John, 1977).
Using populations taken from mine waste and uncontaminated control areas, some authors
have quantified the degree of tolerance of Agrostis tenuis (Karataglis, 1982) and Festuca
rubra (Wong, 1982) under controlled laboratory conditions. Root elongation was used as the
index of tolerance. At 36 pg Pb/g nutrient solution, all populations of A. tenuis were com-
pletely inhibited. At 12 pg Pb/g, the control populations from low lead soils were completely
inhibited, but the populations from mine soils achieved 30 percent of their normal growth
(growth at no lead 1n nutrient solution). At 6 pg/g, the control populations achieved 10 per-
cent of their normal growth, tolerant populations achieved 42 percent. There were no measure-
ments below 6 pg/g. Wong (1982) measured the index of tolerance at one concentration only,
2.5 pg Pb/g nutrient solution, and found that non-adapted papulations of Festuca rubra which
had grown on soils with 47 pg/g total lead content were completely inhibited, populations from
soils with 350 to 650 pg/g achieved 3 to 7 percent of normal growth, and populations from
5,000 |jg/g soil achieved nearly 40 percent of normal growth.
These studies support the conclusion that inhibition of plant growth begins at a lead
concentration of less than 1 pg/g soil moisture and becomes completely Inhibitory at a level
between 3 and 10 pg/g. Plant populations that are genetically adapted to high lead soils may
achieve 50 percent of their normal root growth at lead concentrations above 3 pg/g. These
experiments did not show the effect of reduced root growth on total productivity, but they did
show that exposure to high lead soils is a requirement for genetic adaptation and that, at
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least in the case of F. rubra, plant lead concentrations increase with increasing concentra-
tions in the soil.
8-3-1.4 Effects of Lead on Forage Crops. In the 1977 Criteria Document (U.S. Environmental
Protection Agency, 1977), there was a general awareness that most of the lead in plants was
surface lead from the atmosphere. Most studies since then have addressed the probleu of dis-
tinguishing between surface and internal plant lead. The general conclusion is that, even in
farmlands remote from major highways or industrial sources, 90 to 99 percent of the total
plant lead is of anthropogenic origin (National Academy of Sciences, 1980). Obviously, the
critical agricultural problem concerns forage crops and leafy vegetables. In Great Britain,
Crump and Barlow (1982) determined that within 50 m of the highway, surface deposition is the
major source of lead in forage vegetation. Beyond this range, seasonal effects can obscure
the relative contribution of atmospheric lead. The atadspheric deposition rate appears to be
much greater in the winter than in the summer. Two factors may explain this difference.
First, deposition rate is a function of air concentration, particle size distribution, wind-
speed, and surface roughness. Of these, only particle size distribution is likely to be inde-
pendent of seasonal effects. Lower windspeeds or air concentration during the summer could
account for lower deposition rates. Second, it may be that the deposition rate only appears
to change during the summer. With an increase in biomass and a greater turnover in biomass,
the effective surface area increases and the rate of deposition, which is a function of sur-
face area, decreases. During the summer, lead may not build up on the surface of leaves as it
does in winter, even though the flux per unit of ground area may be the sane.
8.3.1.5 Summary of Plant Effects. When soil conditions allow lead concentrations in soil
moisture to exceed 2 to 10 pg/g, most plants experience reduced growth due to the inhibition
of one or more physiological processes. Excess calcium or phosphorus may reverse the effect.
Plants that absorb nutrients from deeper soil layers may receive less lead. Acid rain is not
likely to release more lead until after major nutrients have been depleted from the soil. A
few species of plants have the genetic capability to adapt to high lead soils.
8.3.2 Effects on Bacteria and Fungi
8.3.2.1 Effects on Decomposers. Tyler (1972) explained three ways in which lead might inter-
fere with the normal decomposition processes in a terrestrial ecosystem. Lead may be toxic to
specific groups of decomposers, it may deactivate enzymes excreted by decomposers to break
down organic matter, or it may bind with the organic matter to render it resistant to the
action of decomposers. Because lead in litter may selectively Inhibit decomposition by soil
bacteria at 2,000 to 5,000 Mfl/g (Smith, 1981, p. 160), forest floor nutrient cycling processes
may be seriously disturbed near lead smelters (Bisessar, 1982; Watson et al., 1976). This is
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especially Important because approximately 70 percent of plant biomass enters the decomposer
food chain (Swift et al., 1979, p. 6). If decomposition of the biomass 1s Inhibited, then
much of the energy and nutrients remain unavailable to subsequent components of the food
chain. There Is also the possibility that the ability of soil to retain lead would be re-
duced, as humic substances are byproducts of bacterial decomposition.
During decomposition, plant tissues are reduced to resistant particulate matter, as solu-
ble organic and inorganic compounds are removed by the chemical action of soil moisture and
the biochemical action of microorganisms (Odum and Drlfmeyer, 1978). Each group of micro-
organisms specializes 1n the breakdown of a particular type of organic molecule. Residual
waste products of one group become the food for the next group. Swift et al. (1979, p. 101)
explained this relationship as a cascade effect with the following generalized pattern (Figure
8-4). Organisms capable of penetrating hard or chemically resistant plant tissue art the
primary decomposers. These saprotrophs, some of which are fungi and bacteria that reside on
leaf surfaces at the initial stages of senescence, produce a wide range of extracellular
enzymes. Others may reside in the intestinal tract of millipedes, beetle larvae, and termites
capable of mashing plant tissue into small fragments. The feces and remains of this group and
the residual plant tissue are consumed by secondary decomposers, i.e., the coprophiHc fungi,
bacteria, and invertebrates (Including protozoa) specialized for consuming bacteria. These
are followed by tertiary decomposers. Microorganisms usually excrete enzymes that carry out
this digestive process external to their cells. They are often protected by a thick cell
coat, usually a polysaccharide. Because they are interdependent, the absence of one group in
this sequence seriously affects the success of subsequent groups, as well as the rate at which
plant tissue decomposes. Each group may be affected In a different way and at different lead
concentrations. Lead concentrations toxic to decomposer microbes may be as low as 1 to 5 pg/g
or as high as 5,000 pg/g (Doelman, 1978).
Under conditions of mild contamination, the loss of one sensitive bacterial population
may result in its replacement by a more lead-tolerant strain. Inman and Parker (1978) found
that Utter transplanted from a low-lead to a high-lead site decayed more slowly than high-
lead litter, suggesting the presence of a lead sensitive microorganism at the low-lead site.
When high-lead litter was transplanted to the low-lead site, decomposition proceeded at a rate
faster than the low-lead litter at the low-lead site. In fact, the rate was faster than the
high-lead litter at the high-lead site, suggesting even the lead tolerant strains were some-
what inhibited. The long term effect is a change in the species composition of the ecosystem,
which will be considered in greater detail in Section 8.5.2.
Delayed decomposition has been reported near smelters (Jackson and Watson, 1977), mine
waste dumps (Williams et al., 1977), and roadsides (Inman and Parker, 1978). This delay is
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GROUP I
GROUP II
»
GROUP III
INORGANIC
NUTRIENTS
Figure 84. Within the decomposer food chain, detritus is progressively broken down
in a sequence of steps regulated by specific groups of decomposers. Because of the
cascade effect of this process, the elimination of any decomposer Interrupts the sup-
ply of organic nutrients to subsequent groups and reduces the recycling of Inorganic
nutrients to plants. Undecomposed litter would accumulate at the stages preceding
the affected decomposer.
Source; Adapted from Swift et al. (1979).
generally in the breakdown of litter from the first stage (0X) to the second (02) with intact
plant leaves and twigs accumulating at the soil surface. The substrate concentrations at
which lead inhibits decomposition appear to be very low. Williams et al. (1977) found inhibi-
tion in 50 percent of the bacteria and fungal strains at 50 |jg Pb/nl nutrient solution. The
community response time for introducing lead tolerant populations seems very fast, however.
Doe1man and Haanstra (1979a,b) found lead-tolerant strains had replaced non-tolerant bac-
teria within 3 years of lead exposure. These new bacteria were predominately thick-coated
gram negative strains and their effectiveness in replacing lead-sensitive strains was not
evaluated in terms of soil decomposition rates.
Tyler (1982) has also shown that many species of wood-decaying fungi do not accumulate
Pb, Ca, Sr, or Kn as strongly as they do other metals, even the normally toxic metal, cadmium.
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PRELIMINARY.DRAFT
Accumulation was expressed as the ratio of the metal concentration 1n the fungus to Its sub*
strate. A ratio of greater than one Implies accumulation, less than one, exclusion. Of 11
species, Manganese was excluded by ten, strontium by nine, lead by eight, and calcium by
seven. Potassium, at the other end of the spectrum, was not excluded by any species. The
species which appeared to accumulate calcium and lead were described as having harder, less
ephemoral tissues.
This relationship among calcium, strontium, and lead is consistent with the phenomenon of
bi©purification described in Section 8.5.2. From the date of Tyler (1982) it appears that
some of the species of fungi receive lead from a source other than the nutrient medium, per-
haps by direct atmospheric deposition.
8.3.2.2 Effects on Nitrifying Bacteria. The conversion of ammonia to nitrate in soil is a
two-step process mediated by two genera of bacteria, Nitrosomonas and Nitrobacter. Nitrate is
required by all plants, although some maintain a symbiotic relationship with nitrogen-fixing
bacteria as an alternate source of nitrogen. Those which do not would be affected by a loss
of free-living nitrifying bacteria, and It 1s known that many trace metals inhibit this nitri-
fying process (Liang and Tabatabal, 1977,1978). Lead is the least of these, inhibiting nitri-
fication 14 percent at concentrations of 1,000 pg/g soil. Many metals, even the nutrient
metals, manganese and iron, show greater inhibition at comparable molar concentrations.
Nevertheless, soils with environmental concentrations above 1,000 pg Pb/g are frequently found.
Even a 14 percent inhibition of nitrification can reduce the potential success of a plant
population, as nitrate 1s usually the limiting nutrient 1n terrestrial ecosystems. In cul-
tivated ecosystems, nitrification Inhibition is not a problem if nitrate fertilizer is added
to soil, but could reduce the effectiveness of ammonia fertilizer if the crops rely on nitri-
fying bacteria for conversion to nitrates.
8.3.2.3 Methylation by Aquatic Microorganisms. While methyl1ead 1s not a primary form of
environmental lead, methylation greatly increases the toxicity of lead to aquatic organisms
(Wong and Chau, 1979). There is some uncertainty about whether the mechanism of methylation
is biotic or abiotic. Some reports (Wong and Chau, 1979, Thompson and Crerar, 1980) conclude
that lead in sediments can be methylated by bacteria. Reisinger et al. (1981) report that
biomethylatlon of lead under aerobic or anaerobic conditions does not occur and such reports
are probably due to sulfide-induced chemical conversion of organic lead salts. These authors
generally agree that tetranethyl lead can be formed under environmental conditions when
another tetravalent organolead compound is available, but methylation of divalent lead salts
such as Pb(N03)2 does not appear to be significant.
8.3.2.4 Summary of Effects on Microorganisms. It appears that microorganisms are more sen-
sitive than plants to soil lead pollution and that changes in the composition of bacterial
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populations nay be an early Indication of lead effects. Delayed decomposition nay occur at
750 |jg Pb/g soil and nitrification Inhibition at 1,000 Mfl/fl- Many of the environmental vari-
ables which can raise or lower these estimates are not yet known. In certain chemical en-
vironments, the highly toxic tetramethyllead can be formed, but this process does not appear
to be mediated by aquatic microorganisms.
8.4 EFFECTS OF LEAD ON DOMESTIC AND WILD ANIMALS
8.4.1 Vertebrates
8.4.1.1 Terrestrial Vertebrates. Forbes and Sanderson (1978) have reviewed reports of lead
toxicity 1n domestic and wild animals. Lethal toxicity can usually be traced to consumption
of lead battery casings, lead-based paints, oil wastes, putty, linoleum, pesticides, lead shot,
or forage near smelters. Except for lead shot Ingestion, these problems can be solved by pro-
per management of domestic animals. However, the 3,000 tons of lead shot distributed annually
along waterways and other hunting grounds continues to be a problem. Of the estimated 80 to
90 million waterfowl in North America, 3.5 million die of poisoning from lead shot annually
(U.S. Fish and Wildlife Service, 1976).
A single pellet of lead shot weighs about 110 mg, and 70 percent of this may be eroded in
ringed turtle dove gizzards over a period of 14 days (Kendall et al., 1982). Their data
showed an immediate elevation of blood lead and reduction of ALA-D activity within 1 day of
swallowing two pellets.
Awareness of the routes of uptake is important in Interpreting the exposure and accumula-
tion in vertebrates. Inhalation rarely accounts for more than 10 to 15 percent of the dally
intake of lead (National Academy of Sciences, 1980). Much of the inhaled lead 1s trapped on
the walls of the bronchial tubes and passes to the stomach embedded in swallowed mucus.
Because lead in lakes or running stream water is quite low, Intake from drinking water maty
also be insignificant unless the animal drinks from a stagnant or otherwise contaminated
source.
Food 1s the largest contributor of lead to animals. The type of food an herbivore eats
determines the rate of lead Ingestion. More than 90 percent of the total lead in leaves and
bark may be surface deposition, but relatively little surface deposition may be found on some
fruits, berries, and seeds which have short exposure tines. Roots intrinsically have no sur-
face deposition. Similarly, ingestion of lead by a carnivore depends mostly on deposition on
herbivore fur and somewhat less on lead 1n herbivore tissue.
The type of food eaten is a major determinant of lead body burdens 1n small mammals.
Goldsmith and Scanlon (1977) and ScanIon (1979) measured highef lead concentrations 1n Insect-
ivorous species than in herbivorous species, confirming the earlier work of Quarles et al.
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(1974), which showed bocty burdens of granivores < herbivores < Insectivores, and Jeffries and
French (1972) that granivores < herbivores. Animals in these studies were analyzed whole
¦inus the digestive tract. It Is likely that observed diet-related differences were somewhat
diluted by including fur in the analysis, because fur-lead night be similar for snail mammals
from the same habitats with different feeding habits.
Since 1977, there has been a trend away from whole body analyses toward analysis of iso-
lated tissues, especially bones and blood. Bone concentrations of lead are better than blood
as indicators of long tern exposure. Because natural levels of blood lead are not well known
for anlnals and blood is not a good indicator of chronic exposure, blood lead is poorly suited
for estimating total body burdens. One experiment with sheep shows the rapid response of
blood to changes in lead Ingestion and the relative contribution of food and air to the total
blood level. Ward et al. (1978) analyzed the blood in sheep grazing near a highway (0,9 ng/g
al) and in an uncontaainated area (0.2 jjg/nrt). When sheep fro* the uncontaainated area were
allowed to graze near the roadway, their blood levels rose rapidly (within 1 day) to about
3.0 |jg/m1t then decreased to 2.0 pg/ml during the next 2 days, retaining constant for the
remainder of the 14-day period. Sheep from the contaminated area were moved to the uncoir
taminated area, where upon their blood dropped to 0.5 |jg/ml in 10 days and decreased to 0.3
tig/ml during the next 180 days. Sheep in the uncontaminated area that were fed forage from
the roadside experienced an increase in blood lead from 0.2 to 1.1 pg/ml in 9 days. Con-
versely, sheep from the uncontaainated area moved to the roadside but fed forage only from the
uncontaainated site experienced an increase from 0.2 to 0.5 yg/ml in 4 days. These data
show that both air and food contribute to lead in blood and that blood lead concentrations are
a function of both the recent history of lead exposure and the long term storage of lead in
bone tissue.
Chaiiel and Harrison (1981) showed that the highest concentrations of lead occurred in the
bones of small mammals (Table 8-2), with kidney and Hver concentrations somewhat less. They
also showed greater bone concentrations in insectivores than herbivores, both at the control
and contaminated sites. Clark (1979) found lead concentrations in shrews, voles, and brown
bats from roadside habitats near Washington, D.C., to be higher than any previously reported.
His estimates of dosages (7.4 ng Pb/kg«day) exceed those that normally cau$e mortality or
reproductive Impairment in domestic mammals (1.5-9 tag Pb/g-day) (Hammond and Aronson, 1964;
James et al., 1966; Kelliher et al., 1973). Traffic density was the same as reported by Chiliel
and Harrison (1981), nearly twice that of Goldsmith and Scanlon (1977) (See Table 8-2). The
body lead burden of shrews exceeded mice, which exceeded voles. Beresford et al. (1981) found
higher lead 1n box turtles within 500 m of a lead smelter than in those from control sites.
Bone lead exceeded kidney and Hver lead as In saall mammals.
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There are few studies reporting lead in vertebrate tissues fro» remote sites. Ellas et
al. (1976, 1982) reported tissue concentrations in voles, shrews, chipmunks, tree squirrels,
and pine martens fro* the remote High Sierra. Bone concentrations were generally only 2
percent of those reported from roadside studies and 10 percent of the controls of roadside
studies (Table 8-2), indicating the controls were themselves contaminated to a large degree.
Furthermore, biogeochemical calculations suggest that even animals in remote areas have bone
lead concentrations 50 to 500 tines natural background levels. The natural concentration of
lead in the bones of herbivores is about 0.04 ng/g dry weight (Table 8-1). This value nay
vary regionally with geochemical anomalies 1n crustal rock, but provides a reasonable indica-
tor of contamination. Natural levels of lead in carnivore bone tissue should be somewhat
lower, with omnlvores generally in between (Elias and Patterson, 1980; Ellas et al., 1982).
Table 8-2 shows the results of several studies of small animal bone tissue. To convert
reported values to a common basis, assumptions were made of the average water content, calcium
concentration, and average crustal concentration. Because ranges of natural concentrations of
lead in bones, plants, soils, and air are known with reasonable certainty (Table 8-1), it is
possible to estimate the degree of contamination of vertebrates from a wide range of habitats.
It is important to recognize that these are merely estimates that do not allow for possible
errors in analysis or anomalies in regional crustal abundances of lead.
8.4.1.2 Effects on Aouatlc Vertebrates. Two requirements limit the evaluation of literature
reports of lead effects on aquatic organisms. First, any laboratory study should incorporate
the entire life cycle of the organism studied. It is clear that certain stages of a life
cycle are more vulnerable than others (Hodson, 1979, Hodson et al., 1979). For fish, the egg
or fry 1s usually most sensitive. Secondly, the same index must be used to compare results.
Christensen et al. (1977) proposed three indices useful for Identifying the effects of lead on
organisms. A molecular Index reports the maximum concentration of lead causing no significant
biochemical change; residue index is the maximum concentration showing no continuing increase
of deposition in tissue; and a bloassay index is the maximum concentration causing no mortal-
ity, growth change, or physical deformity. These indices are comparable to those of physio-
logical dysfunction (molecular, tissue, and organismic) discussed in Section 8.1.4.
From the standpoint of environmental protection, the most useful index is the molecular
index. This Index 1s comparable to the point of initial response discussed previously and is
equivalent to the "safe concentration" originally described by the U.S. Environmental
Protection Agency (Batelle, 1971) as being the concentration that penults normal reproduction,
growth, and all other life-processes of all organisms. It is unfortunate that very few of the
toxicity studies in the aquatic literature report safe concentrations as defined above.
Nearly all report levels at which some or all of the organisms die.
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PRELIMINARY DRAFT
TABLE 8-2. ESTIMATES OF THE DEGREE OF CONTAMINATION OF HERBIVORES,
OMNIVORES, AND CARNIVORES
Data are based on published concentrations of lead in bone tissue (corrected to dry weight as
indicated). Degree of contamination Is calculated as observed/natural Pb. Natural lead con-
centrations are from Table 8-1. Concentrations are 1n |ig Pb/g dw.
Organise
Bone
Pb conc.
Ref.
Estimated degree of
contamination
bone
Herbivores
Vole-roadside 38
Vole-roadside 17
-control 5
Vole-orchard 73
-control 9
Vole-renote 2
Deer House-roadside 25
-control S.7
Deer mouse-roadside 29
-control 7.2
Deer mouse-roadside 52
-control 5
Nouse-roadside 19
-control 9.3
Mouse-roadside 109
-control 18
Average herbivore
roadside (7) 41
control (7) 8.5
remote (2) 2
Dmivores/frugivores
1
2
2
5
5
11
2
2
3
3
4
4
2
2
2
2
320
140
42
610
75
17
210
48
240
60
430
42
160
78
910
150
340
71
17
Moodmouse-roadside
67
1
840
-control
- 25
1
310
Composite-roadside
22
7
280
-control
3
7
37
Chipmunk-remote
2
1
25
Tree squirrel-remote
1.3
11
16
Feral pigeon-urban
670
6
8400
-rural
5.7
6
71
Feral pigeon-urban
250
12
3100
-suburan
33
12
410
-rural
12
12
150
Starling-roadside
210
7
2600
-control
13
7
160
(continued)
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PRELIMINARY DRAFT
TABLE 8-2. (continued)
Organism
Bone
Pb conc.
Ref.
Estimated degree of
contamination
bone
Robin-roadside
130
7
1600
-control
41
7
510
Sparrow-roadside
130
7
1600
-control
17
7
200
Blackblrd-roads1de
90
7
1100
-control
7
7
88
Grackle-roadside
63
7
790
-control
22
7
280
Rats-roadside
310®
9
10000
-control
15
9
500
Average omnlvore
roadside (7)
102
1260
urban (1)
670
8400
control (7)
18
230
remote (2)
1.7
21
Carnivores
Box turtle-smelter
91®
8
3000
-control
5.7
8
190
Egret-rural
12.
10
400
Gull-rural
lla
10
370
Shrew-roadside
67
2
2200
-control
12
2
400
Shrew-roadside
193
1
6400
-control
41
1
1400
Shrew-remote
4.6
1
150
Pine marten-remote
1.4
11
47
Average carnivore
roadside (3)
190
6200
shelter (1)
91
3000
rural (2)
11
385
control (4)
18
620
remote (2)
3
" 99
aDry weight calculated from published fresh wights assuming 35 percent water.
1. Chsrtel and Harrison, 1981
2. Getz et al., 1977b
3. Welch and Dick, 1975
4. Mlerau and Favara, 1975
5. Elfvlng et al., 1978
6. Hutton and Goodman, 1980
7. Getz et al., 1977a
8. Beresford et al., 1981
9. Mouw et al., 1975
10. Hulse et al., 1980
11. Ellas et al., 1982
12. Johnson et al., 1982b
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Hematological and neurological responses are the most commonly reported effects of
extended lead exposures in aquatic vertebrates. Hematological effects include the disabling
and destruction of mature red blood cells and the inhibition of the enzyme AlA-0 required for
hemoglobin synthesis. At low exposures, fish compensate by forming additional red blood
cells. These red blood cells often do net reach maturity. At higher exposures, the fish
become anemic. Symptoms of neurological responses are difficult to detect at low exposure,
but higher exposure can induce neuromuscular distortion, anorexia, and muscle tremors. Spinal
curvature eventually occurs with time or increased concentration (Hodson 1979; Hodson et al.,
1977). Weis and Weis (1982) found spinal curvature in developing eggs of kilUfish when the
embryos had been exposed to 10 pg Pb/ml during the first 7 days after fertilization. All
batches showed some measure of curvature, but those that were most resistant to lead were
least resistant to the effects of methylmercury.
The biochemical changes used by Christensen et al. (1977) to determine the molecular
index for brook trout were 1) increases in plasma sodium and chloride and 2) decreases in
glutamic oxalacetic transaminase activity and hemoglobin. They observed effects at 0.5 pg/1,
which is 20-fold less than the lower range (10 pg/1) suggested by Wong et al. (1978) to cause
significant detrimental effects. Hodson et al. (1978a) found tissue accumulation and blood
parameter changes in rainbow trout at 13 pg/1. This was the lowest experimental level, and
only slightly above the controls, which averaged 4 jjg/1. They concluded, however, that
because spinal curvature does not occur until exposures reach 120 pg/1, rainbow trout are ade-
quately protected at 25 jjg/1.
Aside from the biochemical responses discussed by Christensen et al. (1977), the lowest
reported exposure concentration that causes hematological or neurological effects is 8 (jg/1
(Hodson, 1979). Christensen's group dealt with subcellular responses, whereas Hodson's group
dealt primarily with responses at the cellular or higher level. Hodson et al. (1978a) also
reported that lead in food 1s not available for assimilation by fish, that most of their lead
comes from water, and that decreasing the pH of water (as in acid rain) increases the uptake
of lead by fish (Hodson et al., 1978b). Patrick and Loutit (1978), however, reported that
tissue lead in fish reflects the lead in food if the fish are exposed to the food for more
than a few days. Hodson et al. (1980) also reported that, although the symptoms are similar
(spinal deformation), lead toxicity and ascorbic acid deficiency are not eetabollcally
related.
8.4.2 Invertebrates
Insects have lead concentrations that correspond to those found in their habitat and diet.
Herbivorous invertebrates have lower concentrations than do predatory types (Wade et al.,
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PRELIMINARY DRAFT
1980). Among the herbivorous groups, sucking Insects have lower lead concentrations than
chewing Insects, especially 1n regions near roadsides, where nore lead 1s found on the sur-
faces of vegetation. W11Hanson and Evans (1972) found gradients away from roadsides are not
the sane as with vertebrates, 1n that Invertebrate lead decreases nore slowly than vertebrate
lead relative to decreases 1n soil lead. They also found great differences between major
groups of Invertebrates. Wood lice 1n the same habitat, eating the sane food, had eight tines
more lead than nllllpedes.
The distribution of lead anong terrestrial gastropod tissues was reported by Ireland
(1979). He found little difference among the foot, skin, mantle, digestive gland, gonad, and
Intestine. There are no reports of lead toxicity in soil Invertebrates. In a feeding experi-
ment, however, Coughtrey et al. (1980) found decreased tolerance for lead by microorganisms
fron the guts of insects at 800 MS Pb/g food. Many roadside soils fall 1n this range.
In Cepaea hortensis. a terrestrial snail, Williamson (1979) found nost of the lead in the
digestive gland and gonadal tissue. He also determined that these snails can lose 93 percent
of their whole body lead burden in 20 days when fed a low-lead diet In the laboratory. Since
no analyses of the shell were reported, elimination of lead from this tissue cannot be evalu-
ated. A continuation of the study (Williamson, 1980) showed that body weight, age, and day-
length Influenced the lead concentrations in soft tissues.
Beeby and Eaves (1983) addressed the question of whether uptake of lead 1n the garden
snail, Helix aspersa. is related to the nutrient requirement for calcium during shell forma-
tion and reproductive activity. They found both metals were strongly correlated with changes
1n dry weight and little evidence for correlation of lead with calcium independent of weight
gain or loss. Lead 1n the diet remained constant.
Gish and Chrlstensen (1973) found lead in whole earthworms to be correlated with soil
lead, with little rejection of lead by earthworms. Consequently, animals feeding on earth-
worms from high lead soils might receive toxic amounts of lead in their diets, although there
was no evidence of toxic effects on the earthworms (Ireland, 1977). Ash and Lee (1980)
cleared the digestive tracts of earthworms and still found direct correlation of lead in
earthworms with soil lead; in this case, soil lead was inferred fron fecal analyses. These
authors found differences among species of earthworms. Ireland and Richards (1977) also found
species differences In earthworms, as well as some localization of lead in subcellular organ-
elles of chloragogue and Intestinal tissue. In view of the fact that chloragocytes are be-
lieved to be involved with waste storage and glycogen synthesis, the authors concluded that
this tissue is used to sequester lead 1n the manner of vertebrate livers. Species differences
in whole body lead concentrations could not be attributed to selective feeding or differential
absorption, unless the differential absorption occurs only at elevated lead concentrations.
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PRELIMINARY DRAFT
The authors suggested that the two species have different Maximum tolerances for body lead but
gave no Indication of physiological dysfunction when the maximum tolerance was reached. In
soils with a total lead concentration of 1,800 pg/g dry weight (Ireland, 1975), Lumbricus
rubellus had a whole body concentration of 3,600 pg/g> while Oendrobaene rubida accumulated
7,600 pg/g in the sane location (Ireland and Richards, 1977). Because this difference was not
observed at the control site (15 pg/g soil), it can be assumed that at some soil concentration
between 15 and 1,800 pg/g, different species of earthworms begin to accumulate different
amounts of lead. The authors concluded that D. rubida can simply tolerate higher tissue lead
concentrations, implying that soil concentrations of 1,800 pg/g are toxic to L. rube11 us. This
concentration would be considerably lower than soil lead concentrations that cause effects in
plants, and similar to that which can affect soil microorganisms.
Aquatic insects appear to be resistant to high levels of lead in water. To be conclu-
sive, toxicity studies must observe invertebrates through an entire life cycle, although this
is Infrequently done. Anderson et al. (1980) found LCS0's for eggs and larvae of Tanytarsus
dissimilis, a chironomid, to be 260 pg/1. This value 1s 13 to 250 times lower than previously
reported by Warnick and Bell (1969), Rehwoldt et al. (1973), and Nehring (1976). However,
Spehar et al. (1978) found that mature amphipods (Gammarus pseudolimnaeus) responded nega-
tively to lead at 32 pg/1, Fraser et al. (1978) found that adult populations of a freshwater
isopod (Asellus aquaticus) have apparently developed a genetic tolerance for lead in river
sediments.
Newman and Mcintosh (1982) investigated freshwater gastropods, both grazing and burrow-
ing. Lead concentrations in the grazers (Physa integra. Pseudosuccinea columella, and Helisoma
trivolvis) were more closely correlated with water concentrations than with lead 1n the food.
Lead-in the burrowing species, Campeloma decisun. was not correlated with any environmental
factor. These authors (Newman and Mcintosh, 1983) also reported that both Physa integra and
Caapeloma decisurn are able to eliminate lead from their soft tissue when transferred to a
low-lead medium, but that tissue lead stabilized at a level higher than found in populations
living permanently in the low-lead environment. This would seem to indicate the presence of a
persistent reservoir of lead in the soft tissues of these gastropods.
Borgmann et al. (1978) found increased mortality 1n a freshwater snail, lyanaea palutris.
associated with stream water with a lead content as low as 19 pg/1. Full life cycles were
studied to estimate population productivity. Although individual growth rates were not af-
fected, increased mortality, especially at the egg hatching stage, effectively reduced total
biomass production at the population level. Production was 50 percent at 36 pg/1 and 0 per-
cent at 48 pg Pb/1.
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PRELIMINARY DRAFT
The relationship between LC60 and Initial physiological response 1s not immediately
obvious. It is certain that some Individuals of a population experience physiological dys-
function well before half of then die. For example, B1es1nger and Chrlstensen (1972) observed
minimum reproductive Impairment 1n Paphnla at 6 percent of the LC60 (450 jig/1) for this
species.
8.4.3 Summary of Effects on Animals
While it Is Impossible to establish a safe llnlt of dally lead consumption, it 1s reason-
able to generalize that a regular diet of 2 to 8 mg Pb/kg*day body weight over an extended
period of time (Botts, 1977) will cause death In most animals. Animals of the grazing food
chain are affected most directly by the accumulation of aerosol particles on vegetation sur-
faces and somewhat Indirectly by the uptake of lead through plant roots. Many of these
animals consume more than 1 ng Pb/kg*day 1n habitats near smelters and roadsides, but no toxic
effects have been documented. Animals of the decomposer food chain are affected Indirectly by
lead in soil which can eliminate populations of microorganisms proceeding animals 1n the food
chain or occupying the digestive tract of animals and aiding 1n the breakdown of organic
matter. Invertebrates may also accumultate lead at levels toxic to their predators.
Aquatic animals are affected by lead at water concentrations lower than previously con-
sidered safe (50 Mg Pb/1) for wildlife. These concentrations occur commonly, but the contri-
bution of atmospheric lead to specific sites of high aquatic lead 1s not clear.
8.5 EFFECTS OF LEAD ON ECOSYSTEMS
There is wide variation In the mass transfer of lead from the atmosphere to terrestrial
ecosystems. Even within the somewhat artificial classification of undisturbed, cultivated,
and urban ecosystems, reported fluxes in undisturbed ecosystems vary by nearly 20-fold. Smith
and Siccana (1981) report 270 g/ha-yr in the Hubbard Brook forest of New Hampshire; Lindberg
and Harris# (1981) found 50 g/ha-yr in the Walker Branch watershed of Tennessee; and Ellas et
al. (1976) found 15 g/ha-yr in a remote subalplne ecosystem of California. Jackson and Watson
(1977) found 1,000,000 g/ha-yr near a smelter in southeastern Missouri. Get2 et al. (1979)
estimated 240 g/ha-yr by wet precipitation alone in a rural ecosystem largely cultivated and
770 g/ha-yr In an urban ecosystem.
One factor causing great variation is remoteness from source, which translates to lower
air concentrations, smaller particles, and greater dependence on wind as a nechanlsm of depo-
sition (Ellas and Oavidson, 1980). Another factor is type of vegetation cover. Oeciduous
leaves may, by the nature of their surface and orientation in the wind stream, be nore suit-
able deposition surfaces than conifer needles. Davidson et al. (1982) discussed the influence
of leaf surface on deposition rates to grasses.
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PRELIMINARY DRAFT
The history of lead contamination 1n roadside ecosystems has been reviewed by Smith
(1976). Recent studies have shown three areas of concern where the effects of lead on eco-
systems may be extremely sensitive (Martin and Coughtrey, 1981; Smith, 1981). First, decor-
position is delayed by lead, as some decomposer microorganisms and invertebrates are inhibited
by soil lead. Secondly, the natural processes of calcium biopuriflcation are circumvented by
the accumulation of lead on the surfaces of vegetation and In the soil reservoir. Thirdly,
some ecosystems experience subtle shifts toward lead tolerant plant populations. These pro-
blems all arise because lead in ecosystems Is deposited on vegetation surfaces, accumulates in
the soil reservoir, and is not removed with the surface and ground water passing out of the
ecosystem. Other potential effects are discussed that may occur because of the longtern
build-up of lead in soil.
8.5.1 Delayed Decomposition
The flow of energy through an ecosystem is regulated largely by the ability of organisms
to trap energy in the form of sunlight and to convert this energy from one chemical form to
another (photosynthesis). Through photosynthesis, plants convert light to stored chemical
energy. Starch is only a minor product of this energy conversion. The most abundant sub-
stance produced by net primary production is cellulose, a structural carbohydrate of plants.
Terrestrial ecosystems, especially forests, accumulate a tremendous amount of cellulose as
woody tissue of trees. Few animals can digest cellulose and most of these require symbiotic
associations with specialized bacteria. It is no surprise then, that most of this cellulose
must eventually pass through the decomposer food chain. Utter fall is the major route for
this pathway. Because 80 percent or more of net primary,production passes through the decom-
posing food chain (Swift et al., 1979), the energy of this litter is vital to the rest of the
plant community and the Inorganic nutrients are vital to plants.
The amount of lead that causes litter to be resistant to decomposition 1s not known.
Although laboratory studies show that 50 ytg Pb/ml nutrient medium definitely Inhibits soil
bacterial populations, field studies indicate little or no effect at 600 hq/q Utter (Ooelman
and Haanstra, 1979b). One explanation is that the lead in the laboratory nutrient medium was
readily available, while the lead in the Utter was chemically bound to soil organic matter.
Indeed, Ooelman and Haanstra (1979a) demonstrated the effects of soil lead content on delayed
decomposition: sandy soils lacking organic complexing compounds showed a 30 percent Inhibition
of decomposition at 750 yg/g, including the complete loss of major bacterial species, whereas
the effect was reduced in clay soils and non-existent in peat soils. Organic matter maintains
the cation exchange capacity of soils. A reduction 1n decomposition rate was observed by
Doelman and Haanstra (1979a) even at the lowest experimental concentration of lead, leading to
the conclusion that some effect might have occurred at even lower concentrations.
PB8A/B 8-34 7/13/83
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PRELIMINARY DRAFT
When decomposition is delayed, nutrients may be limiting to plants. In tropical regions
or areas with sandy soils, rapid turnover of nutrients is essential for the success of the
forest community. Even in a mixed deciduous forest, a significant portion of the nutrients,
especially nitrogen and sulfur, may be found in the litter reservoir (Likens et al. 1977).
Annual Utter inputs of calcium and nitrogen to the soil account for about 60 percent of root
uptake. With delayed decomposition, plants must rely on precipitation and soil weathering for
the bulk of their nutrients. Furthermore, the organic content of soil may decrease, reducing
the cation exchange capacity of soil.
8.5.2 Circumvention of Calcium Biopurification
Biopurification is a process that regulates the relative concentrations of nutrient to
non-nutrient elements 1n biological components of a food chain. In the absence of absolute
knowledge of natural lead concentrations, biopurification can be a convenient method for esti-
mating the degree of contamination. Following the suggestion by Comar (1966) that carnivorous
animals show reduced Sr/Ca ratios compared to herbivorous animals which, in turn show less
than plants, Ellas et al. (1976, 1982) developed a theory of biopurification, which hypothe-
sizes that calcium reservoirs are progressively purified of Sr, Ba, and Pb 1n successive
stages of a food chain. In other words, if the Sr/Ca and Ba/Ca ratios are known, the natural
Pb/Ca ratio can be predicted and the observed Pb/Ca to natural Pb/Ca ratio is an expression of
the degree of contamination. Elias et al. (1976, 1982) and Elias and Patterson (1980)
observed continuous biopurification of calcium in grazing and detrital food chains by the pro-
gressive exclusion of Sr, Ba, and Pb (Figure 8-5). It is now believed that members of grazing
and decomposer food chains are contaminated by factors of 30 to 500, i.e., that 97 percent to
99.9 percent of the lead 1n organisms 1s of anthropogenic origin. Burnett and Patterson
(1980) have shown a similar pattern for a marine food chain.
The mechanism of biopurification relies heavily on the selective transport of calcium
across membranes, the selective retention of non-nutrients at physiologically inactive binding
sites, and the reduced solubility of non-nutrient elements in the nutrient medium of plants
and animals. For example, lead 1s bound more vigorously to soil organic complexes and is less
soluble in soil moisture (Section 6.5.1). Lead 1s also adsorbed to cell walls in the root
apoplast, 1s excluded by the cortical cell membrane, and 1s Isolated as a precipitate 1n sub-
cellular vesicles of cortical cells (Koeppe, 1981). Further selectivity at the endodermis
results 1n a nutrient.solution of calcium in the vascular tissue which is greatly purified of
lead. Similar mechanisms occur in the stems and leaves of plants, in the digestive and circu-
latory systems of herbivores and carnivores, and 1n the nutrient processing mechanisms of
Insects.
PB8A/B
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PRELIMINARY DRAFT
10"*
ROCKS SOIL PLANT HERBI CARNI
MOISTURE LEAVES VORES VORES
Figure 8-6. The atomic ratios Sr/Ca, Ba/Ca and Pb/Ca (O)
normally decreese by several orders of magnitude from the
crystal rock to ultimate carnivores In grazer and decomposer
food chains. Anthropogenic laad In soil moisture and on the
surfaces of vegetation and animal fur Interrupt this process
to causa elevated Pb/Ca ratios (•) at each stage of the
sequence. Hie degree of contamination is the ratio of Total
Pb/Ca vs. Natural Pb/Ca at any stage. Ba/Ca and Sr/Ca ratios
are approximate guidelines to the expected natural Pb/Ca
ratio.
PB8A/B
Source: Adapted from Elias at al. (1982).
8-36
7/01/83
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PRJEOMINARY DRAFT
Atmospheric lead circumvents the natural biopurification of calcium. Deposition on plant
surfaces, which accounts for 90 percent of the total plant lead, Increases the ratio of Pb/Ca
in the diet of herbivores. Deposition on animal fur increases the Pb/Ca ratio in the diet of
carnivores. Atmospheric lead consumed by inhalation or grooming, possibly 15 percent of the
total intake of lead, represents sources of lead which were non-existent in prehistoric times
and therefore were not present in the food chain.
8.5.3 Population Shifts Toward Lead Tolerant Populations
It has been observed that plant communities near smelter sites are composed mostly of
lead tolerant plant populations (Antonovics et al., 1971). In some cases, these populations
appear to have adapted to high-lead soils, since populations of the sane species from low-lead
soils often do not thrive on high-lead soils (Jowett, 1954). Similar effects have been ob-
served for soils enriched to 28,000 pg/g dry weight with ore lead (Holland and Oftedal, 1980)
and near roadsides at soil concentrations of 1,300 pg/g dry weight (Atkins et al., 1982). In
these situations, 1t 1s clear that soil lead concentration has become the dominant factor 1n
determining the success of plant populations and the stability of the ecological community.
Soil moisture, soil pH, light intensity, photoperiod, and temperature are all secondary fac-
tors (Antonovics et al., 1971). Strategies for efficient use of light and water, and for
protection from temperature extremes, are obliterated by the succession of lead-tolerant plant
populations. Smith and Bradshaw (1972) concluded that lead-tolerant plant populations of
Festuca rubra and Agrostis tenuis can be used to stabilize toxic mine wastes with lead concen-
trations as high as 80,000 M9/9-
8.5.4 Mass Balance Distribution of Lead In Ecosystems
Inputs of natural lead to ecosystems, approximately 90 percent from rock weathering and
10 percent from atmospheric sources, account for slightly more than the hydrologic lead out-
puts in most watersheds (Patterson, 1980). The difference 1s small and accumulation in the
ecosystem is significant only over a period of several thousand years. In modern ecosystems,
with atmospheric inputs exceeding weathering by factors of 10 to 1000, greater accumulation
occurs 1n soils and this reservoir must be treated as lacking a steady state condition
(Heinrichs and Mayer, 1977, 1980; Siccama and Smith, 1978). Odum and Drifmeyer (1978)
describe the role of detrital particles in retaining a wide variety of pollutant substances,
and this role may be extended to Include non-nutrient substances.
It appears that plant communities have a built-in mechanism for purifying their own
nutrient medium. As a plant community matures through successional stages, the soil profile
develops a stratified arrangement which retains a layer of organic material near the surface.
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PRELIMINARY DRAFT
This organic layer becomes a natural site for the accumulation of lead and other non-nutrient
metals which might otherwise interfere with the uptake and utilization of nutrient metals.
But the rate accumulation of lead in this reservoir may eventually exceed the capacity of the
reservoir. Johnson et al. (1982a) have established a baseline of 80 stations in forests of
the northeast United States. In the litter component of the forest floor, they measured an
average lead concentration of 150 pg/g. Near a smelter, they measured 700 (jg/g and near a
highway, 440 pg/g. They presented some evidence from buried litter that predevelopment con-
centrations were 24 pg/g. On an area basis, the present concentrations range from 0.7 to
1,8 g Pb/m2. Inputs of 270 g/ha-yr measured in the Hubbard Brook forest (see Section 8.5)
would account for 1.0 g Pb/m2 in forty years if all of the lead were retained. The 80 sta-
tions will be monitored regularly to show temporal changes. Evidence for recent changes in
Utter lead concentrations is documented in the linear relationship between forest floor lead
concentration and age of forest floor, up to 100 years.
Lead in the detrital reservoir is determined by the continued input of atmospheric lead
from the litter layer, the passage of detritus through the decomposer food chain, and the rate
of leaching into soil moisture. There is strong evidence that soil has a finite capacity to
retain lead (Zimdahl and Skogerboe, 1977). Harrison et al. (1981) observed that most of the
lead in roadside soils above 200 pg/g is found on Fe-Hn oxide films or as soluble lead car-
bonate. Ellas et al. (1982) have shown that soil moisture lead is derived from the leachable/
organic fraction of soil, not the inorganic fraction. Lead is removed from the detrital
reservoir by the digestion of organic particles in the detrital food chain and by the release
of lead to soil moisture. Both mechanisms result in a redistribution of lead among all of the
reservoirs of the ecosystem at a very slow rate. A closer look at the mechanisms whereby lead
is bound to humic and fulvic acids leads to the following conclusions: 1) because lead has a
higher binding strength than other metals, lead can displace other metals on the organic
molecule (Schnitzer and Khan, 1978); 2) if calcium 1s displaced, it would be leached to a
lower soil horizon (B), where it m«y accumulate as it normally does during the development of
the soil profile; and 3) if other nutrient metals, such as iron or manganese, are displaced,
they may become unavailable to roots as they pass out of the soil system.
Fulvic acid plays an important role in the development of the soil profile. This organic
acid has the ability to remove iron from the lattice structures of Inorganic minerals, result-
ing in the decomposition of these minerals as a part of the weathering process. This break-
down releases nutrients for uptake by plant roots. If all binding sites on fulvic acid art
occupied by lead, the role of fulvic acid in providing nutrients to plants will be circum-
vented. While it is reasonably certain that such a process is possible, there is no informa-
tion about the soil lead concentrations that would cause such an effect.
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Ecosystem Inputs of lead by the atmospheric route have established new pathways and
widened old ones. Insignificant anounts of lead are removed by surface runoff or ground water
seepage. It is likely that the ultimate fate of atmospheric lead will be a gradual elevation
in lead concentration of all reservoirs in the system, with most of the lead accuaulating in
the detrital reservoir.
8.8 SUMMARY
Because there is no protection fro® industrial lead once it enters the atmosphere, it is
important to fully understand the effects of industrial lead emissions. Of the 450,000 tons
emitted annually on a global basis, 115,000 tons of lead fall on terrestrial ecosystems.
Evenly distributed, this would amount to 0.1 g/ha-yr, which is much lower than the range of
15 to 1,000,000 g/ha*yr reported 1n ecosystem studies in the United States. Lead has per-
meated these ecosystems and accumulated in the soil reservoir where it will remain for decades
(Chapter 6). Within 20 meters of every major highway, up to 10,000 pg Pb have been added to
each gram of surface soil since 1930 (Getz et al., 1979). Near smelters, mines, and in urban
areas, as much as 130,000 pg/g have been observed in the upper 2.5 cm of soil (Jennett et al.,
1977). At increasing distances up to 5 kilometers away from sources, the gradient of lead
added since 1930 drops to less than 10 pg/g (Page and Ganje, 1970), and 1 to 5 pg/g have been
added in regions more distant than 5 kilometers (Nriagu, 1978). In undisturbed ecosystems,
atmospheric lead is retained by soil organic matter in the upper layer of soil surface. In
cultivated soils, this lead is mixed with soil to a depth of 25 cm.
Because of the special nature of the soil reservoir, it must not be regarded as an infi-
nite sink for lead. On the contrary, atmospheric lead which is already bound to soil will
continue to pass into the grazing and detrital food chains until equilibrium is reached,
whereupon the lead in all reservoirs will be elevated proportionately higher than natural
background levels. This conclusion applies also to cultivated soils, where lead bound within
the upper 25 cm is still within the root zone.
few plants can survive at soil concentrations in excess of 20,000 pg/g, even under opti-
mum conditions. Some key populations of soil microorganisms and invertebrates die off at 1000
pg/g. Herbivores, in addition to a normal diet from plant tissues, receive lead from the sur-
faces of vegetation in amounts that may be 10 times greater than from internal plant tissue.
A diet of 2 to 8 ag/daykg body weight seems to Initiate physiological dysfunction in many
vertebrates.
Whereas previous reports have focused on possible toxic effects of lead on plants,
animals, and humans, it is essential to consider the degree of contamination as one measure of
safe concentration. Observed toxic effects occur at environmental concentrations well above
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levels that cause no physiological dysfunction. Small animals 1n undisturbed ecosystems are
contaminated by factors of 20 to 600 over natural background levels, and In roadside and urban
ecosystems by 300 to 6200. Extrapolations based on sublethal effects may become reliable when
these measurements can be made with controls free of contamination. The greatest impact may
be on carnivorous animals, which generally have the lowest concentrations of natural lead, and
may thus havet he greatest percent increase when the final equilibrium 1s reached.
Perhaps the most subtle effect of lead is on ecosystems. The normal flow of energy
through the decomposer food chain may be Interrupted, the composition of communities may shift
toward more lead-tolerant populations, and new blogeochemical pathways may be opened, as lead
flows Into and throughout the ecosystem. The ability of an ecosystem to compensate for atmos-
pheric lead Inputs, especially 1n the presence of other pollutants such as acid precipitation,
depends not so much on factors of ecosystem recovery, but on undiscovered factors of ecosystem
stability. Recovery Implies that Inputs of the perturbing pollutant have ceased and that the
pollutant 1s being removed from the ecosystem. In the case of lead, the pollutant is not
being eliminated from the system nor are the Inputs ceasing. Terrestrial ecosystems will
never return to their original, pristine levels of lead concentrations.
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PRELIMINARY DRAFT
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PRELIMINARY DRAFT
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1202-1207,
FQ8KF/A
¦ ttl-««/!•«
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United State*
Environmental Protection
Agency
Environmental Criteria and
AsaMsment Office
Research Triangle Park NC 27711
£om-eo-t/-s, itaxi
EPA-600/8-83-028A
Auguat 1B83
External Review Draft
Reaaarch and Development
Air Quality
Criteria for Lead
Volume III of IV
Review
Draft
(Do Not
Cite or Quote)
LP P
sjiu \t
1
NOTICE
Thia document it a preliminary draft. It ha* not been formally
ralaaaad by EPA and should not at thla slag* be construed to
represent Agency policy. It Is being circulated for comment on Its
technical accuracy and policy implications.
-------
Draft
Do Not Quote or Cite
EPA-600/8-83-028A
August T983
External Review Draft No. 1
Air Quality Criteria
for Lead
Volume III of IV
NOTICE
This document is a preliminary draft. It has not been formally released by EPA and should not at this stage
be construed to represent Agency policy. It is being circulated for comment on its technical accuracy and
policy implications.
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Research Triangle Park, NC 27711
-------
NOTICE
Mention of trad* mmi or cowttrcial products does not constitute
endorsement or recowendatlon for use.
11
-------
ABSTRACT
The document evaluates and assesses scientific Information on the health
and Mlfare effects associated with exposure to various concentrations of lead
in Mblent air. The literature through 1983 has been reviewed thoroughly for
Information relevant to air quality criteria, although the document Is not
Intended as a complete and detailed review of all literature pertaining to
lead. An attempt has been made to Identify the major discrepancies In our
current knowledge and understanding of the effects of these pollutants.
Although this document Is principally concerned with the health and
welfare effects of lead, other scientific data are presented and evaluated 1n
order to provide a better understanding of this pollutant In the environment.
To this end, the document Includes chapters that discuss the chemistry and
physics of the pollutant; analytical techniques; sources, and types of
emissions; environmental concentrations and exposure levels; atmospheric
chemistry and dispersion modeling; effects on vegetation; and respiratory,
physiological, toxlcological, clinical, and epidemiological aspects of human
exposure.
111
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PRELIMINARY DRAFT
CONTENTS
Page
VOLUME I
Chapter 1. Executive Summary and Conclusions 1-1
VOLUME II
Chapter 2. Introduction •. 2-1
Chapter 3. Chemical and Physical Properties 3-1
Chapter 4. Sampling and Analytical Methods for Environmental Lead 4-1
Chapter 5. Sources and Emissions 5-1
Chapter 6. Transport and Transformation 6-1
Chapter 7. Env1ronnental Concentrations and Potential Pathways to Human Exposure .. 7-1
Chapter 8. Effects of Lead on Ecosystems 8-1
VOLUME III
Chapter 9. Quantitative Evaluation of Lead and Biochemical Indices of Lead
Exposure 1n Physiological Media 9-1
Chapter 10. Metabolism of Lead 10-1
Chapter 11. Assessment of Lead Exposures and Absorption 1n Human Populations 11-1
Volume IV
Chapter 12. Biological Effects of Lead Exposure 12-1
Chapter 13. Evaluation of Human Health Risk Associated with Exposure to Lead
and Its Compounds 13-1
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PRELIMINARY DRAFT
TABLE OF CONTENTS
Page
9. QUANTITATIVE EVALUATION OF LEAD AND BIOCHEMICAL INDICES OF LEW) EXPOSURE
IN PHYSIOLOGICAL MEDIA 9-1
9.1 INTRODUCTION 9-1
9.2 DETERMINATIONS OF LEAD IN BIOLOGICAL MEDIA 9-2
9.2.1 Sampling and Sample Handling Procedures for Lead
in Biological Media 9-2
9.2.1.1 Blood Sampling 9-3
9.2.1.2 Urine Sampling . 9-4
9.2.1.3 Hair Sampling 9-4
9.2.1.4 Mineralized Tissue 9-4
9.2.1.5 Sampling Handling in the Laboratory 9-5
9.2.2 Methods of Lead Analysis 9-6
9.2.2.1 Lead Analysis in Whole Blood 9-7
9.2.2.2 Lead in Plasma 9-10
9.2.2.3 Lead in Teeth 9-12
9.2.2.4 Lead in Hair 9-13
9.2.2.5 Lead in Urine 9-13
9.2.2.,6 Lead in Other Tissues 9-14
9.2.3 Quality Assurance Procedures in Lead Analysis 9-15
9.3 DETERMINATION OF ERYTHROCYTE PORPHYRIN (FREE ERYTHROCYTE
PROTOPOPHYRIN, ZINC PROTOPORPHYRIN) 9-19
9.3.1 Methods of Erythrocyte Porphyrin Analysis 9-19
9.3.2 Interlaboratory Testing of Accuracy and Precision in
EP Measurement 9-23
9.4 MEASUREMENT OF URINARY COPROPORPHYRIN 9-24
9.5 MEASUREMENT OF DELTA-AMINOLEVULINIC ACID DEHYDRATASE ACTIVITY 9-24
9.6 MEASUREMENT OF DELTA-AMINOLEVULINIC ACID IN URINE AND OTHER MEDIA 9-26
9.7 MEASUREMENT OF PYRIMIOINE-51-NUCLEOTIDASE ACTIVITY 9-27
9.8 SUMMARY 9-29
9.8.1 Determinations of Lead in Biological Media 9-29
9.8.1.1 Measurements of Lead in Blood 9-29
9.8.1.2 Lead in Plasma 9-31
9.8.1.3 Lead in Teeth 9-31
9.8.1.4 Lead in Hair 9-31
9.8.1.5 Lead in Urine 9-31
9.8.1.6 Lead in Other Tissues 9-32
9.8.1.7 Quality Assurance Procedures in Lead Analyses 9-32
9.8.2 Determination of Erythrocyte Porphyrin (Free Erythrocyte
Protoporphyrin, Zinc Protoporphyrin) 9-33
9.8.3 Measurement of Urinary Coproporphyrin 9-34
9.8.4 Measurement of Delta-Aminolevulinic Acid Dehydratase Activity ....... 9-34
9.8.5 Measurement of Delta-Aminolevullnic Add In Urine and Other Media ... 9-35
9.8.6 Measurement of Pyrimidine-5'-Nucleotidase Activity 9-36
9.9 REFERENCES 9-37
10. METABOLISM OF LEAD 10-1
10.1 INTRODUCTION 10-1
10.2 LEAD ABSORPTION IN HUMANS AND ANIMALS 10-1
10.2.1 Respiratory Absorption of Lead 10-1
10.2.1.1 Human Studies 10-2
10.2.1.2 Animal Studies 10-5
v
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
E5fl*
10.2.2 Gastrointestinal Absorption of Lead 10-6
10.2.2.1 Huaan Studies 10-6
10.2.2.2 Animal Studies 10-10
10.2.3 Percutaneous Absorption of Lead 10-12
10.2.4 Transplacental Transfer of Lead 10-12
10.3 DISTRIBUTION OF LEAD IN HUMANS AND ANIMALS 10-13
10.3.1 Lead in Blood 10-14
10.3.2 Lead Level s 1 n Tissues 10-15
10.3.2.1 Soft Tissues 10-16
10.3.2.2 Mineralizing Tissue 10-19
10.3.3 Chelatable Lead 10-20
10.3.4 Mathematical Descriptions of Physiological Lead Kinetics — 10-22
10.3.5 Aniaal Studies 10-23
10.4 LEAD EXCRETION AND RETENTION IN HUMANS AND ANIMALS 10-24
10.4.1 Human Studies 10-24
10.4.2 Animal Studies 10-28
10.5 INTERACTIONS OF LEAD WITH ESSENTIAL METALS AND OTHER FACTORS 10-31
10.5.1 Human Studies 10-31
10.5.2 Animal Studies 10-33
10.5.2.1 Interactions of Lead with Calcium 10-34
10.5.2.2 Interactions of Lead with Iron 10-38
10.5.2.3 Lead Interactions with Phosphate 10-38
10.5.2.4 Interactions of Lead with Vitamin D 10-39
10.5.2.5 Interactions of Lead with Lipids 10-39
10.5.2.6 Lead Interaction with Protein 10-39
10.5.2.7 Interactions of Lead with Milk Components 10-40
10.5.2.8 Lead Interactions with line and Copper 10-40
10.6 INTERRELATIONSHIPS OF LEAD EXPOSURE, EXPOSURE INDICATORS,
AND TISSUE LEAD BURDENS 10-41
10.6.1 Temporal Characteristics of Internal Indicators
of Lead Exposure 10-41
10.6.2 Biological Aspects of External Exposure-Internal
Indicator Relationships 10-42
10.6.3 Internal Indicator-Tissue Lead Relationships 10-43
10.7 METABOLISM OF LEAD ALKYLS 10-45
10.7.1 Absorption of Lead Alkyls in Humans and Animals — 10-46
10.7.1.1 Gastrointestinal Absorption 10-46
10.7.1.2 Percutaneous Absorption of Lead Alkyls 10-46
10.7.2 Biotransformation and Tissue Distribution of Lead Alkyls ........... 10-46
10.7.3 Excretion of Lead Alkyls • 10-48
10.8 SUMMARY 10-49
10.8.1 Lead Absorption 1n Humans and Animals 10-49
10.8.1.1 Respiratory Absorption of Lead 10-49
10.8.1.2 Gastrointestinal Absorption of Lead 10-50
10.8.1.3 Percutaneous Absorption of Lead 10-51
10.8.1.4 Transplacental Transfer of Lead 10-51
10.8.2 Distribution of Lead in Humans and Animals 10-51
10.8.2.1 Lead In Blood 10-51
10.8.2.2 Lead Levels in Tissues 10-52
10.8.3 Lead Excretion and Retention 1n Humans and Animals 10-54
10.8.3.1 Human Studies 10-54
v1
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued).
Paoe
10.8.3.2 AtllMl Studies 10-55
10.8.4 Interactions of Lead with Essential Metals and Other Factors ....... 10-56
10.8.4.1 Hunan Studl es 10-56
10.8.4.2 Anlaal Studies 10-56
10.8.5 Interrelationships of Lead Exposure with Exposure Indicators
and Tissue Lead Burdens 10-57
10.8.5.1 Temporal Characteristics of Internal Indicators of
Lead Exposure 10-57
10.8.5.2 Biological Aspects of External Exposure-Internal
Indicator Relationships 10-58
10.8.5.3 Internal Indicator-Tissue Lead Relationships 10-58
10.8.6 Ketabol1sa of Lead Alkyls . 10-59
10.8.6.1 Absorption of Lead Alkyls 1n Husans and ArImIs .......... 10-59
10.8.6.2 Biotransformation and Tissue Distribution of
Lead Alkyls 10-59
10.8.6.3 Excretion of Lead Alklys 10-59
10.9 REFERENCES 10-60
11. ASSESSMENT OF LEAD EXPOSURES AND ABSORPTION IN HUMAN POPULATIONS 11-1
11.1 INTRODUCTION 11-1
11.2 METHODOLOGICAL CONSIDERATIONS 11-4
11.2.1 Analytical Problems 11-4
11.2.2 Statistical Approaches 11-5
11.3 LEAD IN HUMAN POPULATIONS 11-6
11.3.1 Introduction 11-6
11.3.2 Ancient and Reawte Populations (Low Lead Exposures) 11-6
11.3.2.1 Ancient Populations 11-8
11.3.2.2 Renote Populations 11-8
11.3.3 Levels of Lead and Demographic Covariates 1n U.S. Populations 11-10
11.3.3.1 The NHANES II Study 11-10
11.3.3.2 The Childhood Blood Lead Screening Programs 11-15
11.3.4 T1«e Trends 11-19
11.3.4.1 Ti«e Trends in the Childhood Lead Poisoning Screening
Progress 11-19
11.3.4.2 Newark 11-22
11.3.4.3 Boston 11-24
11.3.4.4 NHANES II 11-24
11.3.4.5 Other Studies 11-24
11.3.5 Distributional Aspects of Population Blood Lead Levels 11-24
11.3.6 Exposure Covariates of Blood Lead Levels 1n Urban Children ......... 11-31
11.3.6.1 Stark Study 11-32
11.3.6.2 Charney Study 11-33
11.3.6.3 Haaaond Study 11-34
11.3.6.4 Gilbert Study 11-35
11.4 STUDIES RELATING EXTERNAL DOSE TO INTERNAL EXPOSURE 11-36
11.4.1 Air Studies 11-37
11.4.1.1 The Griffin et al. Study 11*38
11.4.1.2 The RaMnowltz et al. Study 11-47
11.4.1.3 The Charter lain et al. Study 11-50
11.4.1.4 The Kehoe Study ...» 11-52
11.4.1.5 The Azar et al. Study U-53
vii
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PRELIMINARY DRAFT
TABLE OF CONTENTS (continued)
Page
11.4.1.6 Silver Valley/Kellogg, Idaho Study 11-58
11.4.1.7 Omaha, Nebraska Studies 11-65
11.4.1.8 RoeIs et al. Studies 11-6?
11.4.1.9 Other Studies Relating Blood Lead Levels to
Air Exposure 11-70
11.4.1.10 Summary of Blood Lead vs. Inhaled Air Lead Relations ..... 11-74
11.4.2 Dietary Lead Exposures Including Water 11-80
11.4.2.1 Lead Ingestion from Typical Diets — 11-81
11.4.2.2 Lead Ingestion from Experimental Dietary Supplements 11-90
11.4.2.3 Inadvertent Lead Ingestion Fro* Lead Plumbing 11-93
11.4.2.4 Summary of Dietary Lead Exposures Including Water 11-97
11.4.3 Studies Relating Lead in Soil and Dust to Blood Lead 11-105
11.4.3.1 Omaha Nebraska Studies 11-105
11.4.3.2 The Stark Study 11-106
11.4.3.3 The Silver Valley/Kellogg Idaho Study 11-106
11.4.3.4 Charleston Studies 11-106
11.4.3.5 Barltrop Studies 11-107
11.4.3.6 The British Columbia Studies 11-108
11.4.3.7 Other Studies of Soil and Dusts 11-109
11.4.3.8 Summary of Soil and Dust Lead 11-113
11.4.4 Paint Lead Exposures 11-115
11.5 SPECIFIC SOURCE STUDIES 11-121
11.5.1 Combustion of Gasoline Antiknock Compounds 11-121
11.5.1.1 Isotope Studies 11-121
11.5.1.2 Studies of Childhood Blood Lead Poisoning
Control Programs 11-130
11.5.1.3 NHANES II 11-133
11.5.1.4 Frankfurt, West Germany 11-136
11.5.2 Primary Smelters Populations 11-137
11.5.2.1 El Paso, Texas 11-137
11.5.2.2 C0C-EPA Study 11-139
11.5.2.3 Neza Valley, Yugoslavia 11-139
11.5.2.4 Kosovo Province, Yugoslavia 11-140
11.5.2.5 The Cavalleri Study 11-141
11.5.3 Battery Plants 11-142
11.5.4 Secondary Smelters 11-145
11.5.5 Secondary Exposure of Children 11-145
11.5.6 Miscellaneous Studies 11-152
11.5.6.1 Studies Using Indirect Measures of Air Exposure 11-152
11.5.6.2 Miscellaneous Sources of Lead 11-156
11.6 SUMMARY 11-158
11.7 REFERENCES 11-166
APPENDIX 11A 11A-1
APPENDIX 11B 118-1
APPENDIX 11C 11C-1
APPENDIX 11D 110-1
v11i
TCPBA/K 8/8/83
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PRELIMINARY DRAFT
LIST OF FIGURES
Figure Page
10-1 Effect of particle size on lead deposition rate in the lung 10-4
11-1 Pathways of lead from the environment to man 11-3
11-2 Estimate of world-wide lead production and lead concentrations in
bones (pg/gm) from 5500 years before present to the present tine 11-7
11-3 Geometric mean blood lead levels by race and age for younger children
in the NHANES II study 11-16
11-4 Geometric means for blood lead values by race and age for younger
children in the New York City screening program (1970-1976) 11-20
11-5 Time dependence of blood lead for blacks, aged 24 to 35 months,
in New York City and Chicago 11-23
11-6 Modeled umbilical cord blood lead levels by date of sample collection
for infants in Boston 11-25
11-7 Average blood lead levels of U.S. population 6 months * 74 years,
United States, February 1976 - February 1980, based on dates of
examination of NHANES II examinees with blood lead determinations 11-26
11-8 Histograms of blood lead levels with fitted lognormal curves for
the NHANES II study 11-30
11-9 Graph of the average normalized increase in blood lead for subjects
exposed to 10.9 g/m3 of lead in the Griffin et al. study 11-41
11-10 Control subjects in Griffin experiment at 3.2 pg/m3 11-42
11-11 Data plots for individual subjects with time for Kehoe data as
presented by Gross 11-54
11-12 Blood lead vs. air lead relationships for Kehoe inhalation studies:
linear relation for low exposures, quadratic for high exposures, with
95 percent confidence bands 11-55
11-13 Monthly ambient air lead concentrations in Kellogg, Idaho,
1971 through 1975 11-59
11-14 Fitted equations to the Kellogg, Idaho/Silver Valley adjusted
blood lead data 11-64
11-15 Blood-lead concentrations vs. weekly lead intake for bottle-
fed infants 11-87
11-17 Average Pb level, exp. I 11-91
11-18 Average PbB levels, exp. II 11-91
11-19 Lead in blood (mean values and range) in volunteers 11-93
11-20 Cube root regression of blood lead on first flush water lead 11-96
11-21 Relation of blood lead (adult female) to first flush water lead
in combined estates 11-98
11-22 Cumulative distribution of lead levels in dwelling units 11-117
11-23 Correlation of children's blood lead levels with fractions of surfaces
within a dwelling having lead concentrations 22 mg pb/cm2 11-119
11-24 Change in 266Pb/*67Pb ratios in petrol, airborne particulate
and blood from 1974 to 1981 11-123
11-25 Direct and Indirect contributions of lead in gasoline to blood
lead in Italian men 11-126
11-26 Geometric mean blood lead levels of New York City children (aged 25-36
months) by ethnic group, and ambient air lead concentration vs.
quarterly sampling period, 1970-1976 11-131
11-27 Geometric mean blood lead levels of New York City children (ages 25-36
months) by ethnic group, and estimated amount of lead present in
gasoline sold in New York, New Jersey, and Connecticut vs.
quarterly sampling period, 1970-1976 11-132
ix
TCPBA/K 8/8/83
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PRELIMINARY DRAFT
LIST OF FIGURES (continued).
Figure Page
11-28 Geometric mean blood levels for blacks and Hispanlcs In the 25-to-36-
»onth age group and rooftop quarterly averages for anbient cltywlde
lead levels 11-134
11-29 Tt*e dependence of blood lead and gas lead for blacks, ages 24 to 35
Months, in New York 11-135
11-30 Arithmetic mean air lead levels by traffic voluae, Dallas, 1976 11-154
11-31 Blood lead concentration and traffic density by sex and age, Dallas, 1976 11-155
11-32 Geometric «ean blood lead levels by race and age for younger children in
the NHANES II study, and the Kellogg/Silver Valley and the New York
childhood screening studies 11-159
11B-1 Residual sum of squares for nonlinear regression nodels for Azar data
(N=149) 11-170
11B-2 Hypothetical relationship between blood lead and air lead by inhalation
and non-inhalation 11-172
TCPBA/K
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PRELIMINARY DRAFT
LIST OF TABLES
Table Page
10-1 Deposition of lead 1n the human respiratory tract . 10-3
10-2 Regional distribution of lead in hunans and animals 10-17
10-3 Comparative excretion and retention rates 1n adults and Infants 10-25
10-4 Effect of nutritional factors on lead uptake In animals 10-3S
11-1 Studies of past exposures to lead 11-9
11-2 NHANES II blood lead levels of persons 6 months-74 years, with weighted
arithnetic mean, standard error of the mean, weighted geometric mean,
median, and percent distribution, by race and age, United States,
1978-80 11-12
11-3 NHANES II blood lead levels of males 6 months-74 years, with weighted
arithmetic mean, standard error of the mean, weighted geometric mean,
median, and percent distribution, by race and age, United States,
1976-80 11-13
11-4 NHANES II blood lead levels of females 6 roonths-74 years, with weighted
arithmetic mean, standard error of the mean, weighted geometric mean,
median, and percent distribution, by race and age, United States,
1976-80 11-14
11-5 Weighted geometric mean blood lead levels from NHANES II survey by
degree of urbanization of place of residence in the U.S. by age
and race, United States 1978-80 11-17
11-6 Annual geometric mean blood lead levels from the New York blood lead
screening studies. Annual geometric means are calculated from
quarterly geometric means estimated by the method of
Hasselblad et al. (1980) 11-18
11-7 Characteristics of childhood lead poisoning screening data 11-21
11-8 Distribution of blood lead levels for 13 to 48 month old blacks
by season and year for New York screening data 11-21
11-9 Summary of unweighted blood lead levels in whites not living in an
SMSA with family Income greater than $6,000 11-28
11-10 Summary of fits to NHANES II blood lead levels of whites not
living in an SMSA, Income greater than $6,000, for five
different two parameter distributions 11-29
11-11 Estimated mean square errors resulting from analysis of variance on
various subpopulations of the NHANES II data using unweighted data 11-31
11-12 Multiple regression models for blood lead of children in
New Haven, Connecticut, September 1974 - February 1977 11-33
11-13 Griffin experiments - subjects exposed to air lead both years 11-43
11-14 Griffin experiments - controls used both years .... 11-44
11-15 Griffin experiment - subjects exposed to air lead one year only 11-45
11-16 Inhalation slope estimates 11-47
11-17 Mean residence time in blood 11-47
11-18 Air lead concentrations (jjg/m3) for two subjects in the
Rabinowltz studies 11-48
11-19 Estimates of inhalation slope for Rablnowitz studies 11-49
11-20 Linear slope for blood lead vs. air lead at low air lead
exposures in Kehoe's subjects 11-53
11-21 Geometric mean air and blood lead levels (pg/100 g) for five city-
occupation groups 11-56
11-22 Geometric mean blood lead levels by area compared with estimated
air-lead levels for 1- to 9-year-old children living near Idaho
smelter 11-61
xi
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PRELIMINARY DRAFT
LIST OF TABLES (continued).
Table Page
11-23 Geometric mean blood lead levels by age and area for subjects
living near the Idaho smelter 11-61
11-24 Age specific regression coefficients for the analysis of log-blood-
lead levels in the Idaho smelter study 11-62
11-25 Estimated coefficients and standard errors for the Idaho
smelter study 11-63
11-26 Air, dustfall and blood lead concentrations in Omaha, NE, study,
1970-1977 U-66
11-27 Mean airborne and blood lead levels recorded during five distinct
surveys (1974 to 1978) for study populations of 11-year old
children living less than 1 km or 2.5 km from a lead smelter,
or living in a rural or urban area 11-69
11-28 Geometric mean air and blood lead values for 11 study populations 11-71
11-29 Mean air and blood lead values for five zones in Tokyo study 11-71
11-30 Blood lead-air lead slopes for several population studies as
calculated by Snee 11-73
11-31 A selection of recent analyses on occupational 8-hour exposures
to high air lead levels ,. 11-74
11-32 Cross-sectional observational study with measured individual air
lead exposure — 11-75
11-33 Cross-sectional observational studies on children with estimated
air exposures 11-76
11-34 Longitudinal experimental studies with measured individual
air lead exposures 11-77
11-35 Blood lead levels and lead intake values for Infants
in the study of Ryu et al 11-82
11-36 Influence of level of lead in water on blood lead level in
blood and placenta 11-84
11-37 Blood lead and kettle water lead concentrations for adult
women living in Ayr 11-85
11-38 Relationship of blood lead (ug/dl) and water lead (pg/1) in 910
men aged 40-59 from 24 British towns 11-88
11-39 Dose response analysis for blood leads in the Kehoe study as
analyzed by Gross 11-90
11-40 Blood lead levels of 771 persons in relation to lead content of
drinking water, Boston, Mass 11-99
11-41 Studies relating blood lead levels (yg/dl) to dietary intakes (pg/day) 11-100
11-42 Studies relating blood lead levels (pg/dl) and experimental
dietary intakes 11-101
11-43 Studies relating blood lead levels (pg/dl) to
first-flush water lead 11-102
11-44 Studies relating blood lead levels (pg/dl) to running water
lead (pg/1) 11-104
11-45 Mean blood and soil lead concentrations in English stucty 11-108
11-46 Lead concentration of surface soil and children's blood
by residential area of trail, British Columbia 11-110
11-47 Analysis of relationship between soil lead and blood lead in children 11-113
11-48 Estimates of the contribution of soil lead to blood lead .< 11-114
11-49 Estimates to the contribution of housedust to blood lead in children 11-115
11-50 Results of screening and housing inspection in childhood lead
poisoning control project by fiscal year 11-120
xi 1
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PRELIMINARY DRAFT
LIST OF TABLES (continued).
Table Page
11-51 Estimated contribution of leaded gasoline to blood lead by Inhalation
and non-inhalation pathways 11-124
11-52 Assumed air lead concentration for node! 11-125
11-53 Regression model for blood lead attributable to gasoline 11-127
11-54 Rate of change of 26®Pb/204Pb and 26®Pb/207Pb in air and blood, and
percentage of airborne lead 1n blood of subjects 1, 3, 5, 6 and 9 11-128
11-55 Calculated blood lead uptake from air lead using Manton isotope study .......... 11-129
11-56 Mean air lead concentrations during the various blood sampling periods
at the measurement sites described in the text (pg/m3) 11-136
11-57 Mean blood lead levels in selected Yugoslavian populations, by
estimated weekly tine-weighted air lead exposure 11-140
11-58 Environmental parameters and methods: Arnhen lead study, 1978 11-144
11-59 Geometric mean blood lead levels for children based on reported
occupation of father, history of pica, and distance of residence
from smelter 11-146
11-60 Sources of lead 11-157
11-61 Sunwary of pooled geometric standard deviations and estimated
analytic errors 11-160
11-62 Summary of blood inhalation slopes, (P)pg/dl per Mg/m3 11-161
11-63 Estimated contribution of leaded gasoline to blood lead by
Inhalation and non-inhalation pathways 11-165
TCPBA/K
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8/8/83
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS
AAS
Ach
ACTH
ADCC
ADP/O ratio
AIDS
AIHA
All
ALA
ALA-D
ALA-S
ALA-U
APDC
APHA
ASTM
ASV
ATP
B-cells
Bi
BAL
BAP
BSA
BUN
BW
C.V.
CaBP
CaEDTA
CBD
Cd
CDC
CiC
CEH
CFR
CHP
CNS
CO
com
CP-U
cB*h
D.F.
DA
OCHU
DDP
DNA
DTK
EEC
EEG
EMC
EP
EPA
Atomic absorption spectrometry
Acetylcholine
Adrenoeoticotrophlc hormone
Antibo
-------
PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
FA Fulvlc acid
FDA Food and OrKg Administration
Fe Iron
FEP Free erythrocyte protoporphyrin
FY Fiscal year
G.M. Grand itean
G-6-PD G1ucose-6-phosphate dehydrogenase
GABA Gan«a-a«1 rwbutyr 1 c add
SALT Gut-associated lymphoid tissue
GC Gas chromatography
GFR Glomerular filtration rate
HA Humic acid
Hg Mercury
h1-vol High-volume air sampler
HPIC High-performance liquid chromatography
i.m. Intramuscular (method of injection)
i.p. Intraperitoneal^ (method of injection)
i.v. Intravenously (method of Injection)
IAA Indol-3-ylacetic acid
IARC International Agency for Research on Cancer
ICD International classification of diseases
ICP Inductively coupled plasma
IDMS Isotope dilution mass spectrometry
IF Interferon
HE Isotopic Lead Experiment (Italy)
IRPC International Radiological Protection Commission
K Potassium
LAI Leaf area index
LDH-X Lactate dehydrogenase isoenzyme x
LCbq Lethyl concentration (50 percent)
LOr: Lethal dose (50 percent)
LH Luteinizing hormone
LIPO Laboratory Improvement Program Office
In National logarithm
LPS Lipopolysaccharide
LRT Long range transport
mRNA Messenger ribonucleic add
ME Mercaptoethanol
MEPP Miniature end-plate potential
MES Maximal electroshock seizure
MeV Hega-electron volts
MIC Mixed lymphocyte culture
MMD Mass median diameter
MMEO Mass median equivalent diameter
Mn Manganese
HND Motor neuron disease
MSV Moloney sarcoma virus
MTD Maximum tolerated dose
n Number of subjects
N/A Not Available
TCPBA/D
xv 8/8/83
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS
NA Not Applicable
NAAQS National ambient air quality standards
NADS National Aerometric Data Bank
NAMS National Air Monitoring Station
NAS National Academy of Sciences
NASN National Air Surveillance Network
NBS National Bureau of Standards
NE Norepinephrine
NFAN National Filter Analysis Network
NFR-82 Nutrition Foundation Report of 1982
NHANES II National Health Assessment and Nutritional Evaluation Survey II
Ni Nickel
OSHA Occupational Safety and Health Administration
P Potassium
p Significance symbol
PAH Para-aminohippuric acid
Pb lead
PBA Air lead
Pb(Ac), Lead acetate
PbB concentration of lead in blood
PbflrCl Lead (II) bromochloride
PBG Porphobilinogen
PFC Plaque-forming cells
pH Neasure of acidity
PHA Phytohemagglutinin
PHZ Polyacrylami de-hydrous-zirconi a
PIXE Proton-induced X-ray emissions
PMN Polymorphonuclear leukocytes
PND Post-natal day
PNS Peripheral nervous system
ppm Parts per million
PRA Plasma renin activity
PRS Plasma renin substrate
PVIM Pokeweed mitogen
Py-5-N Pyrimide-5'-nucleotidase
RBC Red blood cell; erythrocyte
RBF Renal blood flow
RCR Respiratory control ratios/rates
redox Oxidation-reduction potential
RES Reticuloendothelial system
RLV Rauscher leukemia virus
RNA Ribonucleic acid
S-HT Serotonin
SA-7 Sinian adenovirus
sen Standard cubic meter
S.D. Standard deviation
SOS Sodium dodecyl sulfate
S.E.M. Standard error of the mean
SES Socioeconomic status
5G0T Serum glutamic oxaloacetic transaminase
xvi
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PRELIMINARY DRAFT
LIST OF ABBREVIATIONS (continued).
slg
SLAMS
SMR
Sr
SRBC
SRMs
STEL
SW voltage
T-cells
t-tests
T8L
TEA
TIL
TIBC
TML
TMLC
TSH
TSP
U.K.
UMP
USPHS
VA
fal
UNO
XIF
r
In
ZPP
Surface immunoglobulin
State and local air Monitoring stations
Standardized mortality ratio
Strontium
Sheep red blood cells
Standard reference materi als
Short-tern exposure Unit
Slow-wave voltage
Thynius-derived lymphocytes
Tests of significance
Tri-n-butyl lead
Tetraethyl-ammonium
Tetraethyllead
Total iron binding capacity
Tetramethyllead
Tetramethyllead chloride
Thyroid-stimulating hormone
Total suspended particulate
United Kingdom
Uridine monophosphate
U.S. Public Health Service
Veterans Administration
Deposition velocity
Visual evoked response
World Health Organization
X-Ray fluorescence
Chi squared
Zinc
Erythrocyte zinc protoporphyrin
MEASUREMENT ABBREVIATIONS
dl deciliter
ft feet
g gran
g/gal gram/gallon
g/ha-mo gram/hectare-month
km/hr kilometer/hour
1/mln Hter/nlnute
•g/kM ml111gran/kiloneter
Mfl/m3 microgram/cubic meter
am millimeter
limol micrometer
ng/cm* nanograms/square centimeter
nm rtamooeter
nM nanonole
sec second
TCPBA/D
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AUTHORS, CONTRIBUTORS, AND REVIEWERS
Chapter 9: Quantitative Evaluation of Lead and Biochemical Indices of lead
Exposure in Physiological Media
Principal Author
Dr. Paul Mushak
Department of Pathology
School of Medicine
University of North Carolina
Chapel Hill, NC 27514
The following persons reviewed this chapter at EPA's request. The evaluations
and conclusions contained herein, however, are not necessarily those of the
reviewers.
Dr. Carol Angle
Department of Pediatrics
University of Nebraska
College of Medicine
Omaha, NE 68105
Dr. Lee Annest
Division of Health Examin. Statistics
National Center for Health Statistics
3700 East-West Highway
Hyattsville, MD 20782
Dr. A. C. Chamberlain
Environmental and Medical
Sciences Division
Atomic Energy Research
Establishment
Harwell 0X11
England
Dr. Neil Chernoff
Division of Developmental Biology
MD-67
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Donald Barltrop
Department of Child Health
Westminister Children's Hospital
London SW1P 2NS
England
Or. Irv Billick
Gas Research Institute
8600 West Bryn Mawr Avenue
Chicago, IL 60631
Or. Joe Boone
Clinical Chemistry and
Toxicology Section
Centers for Disease Control
Atlanta, GA 30333
Dr. Robert Bornschein
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 4S267
Dr. Julian Chisoln
Baltimore City Hospital
4940 Eastern Avenue
Baltimore, M0 21224
Mr. Jerry Cole
International Lead-Zinc Research
Organization
292 Madison Avenue
New York, NY 10017
Dr. Max Costa
Department of Pharmacology
University of Texas Medical
School
Houston, TX 77025
Or. Anita Curran
Commissioner of Health
Westchester County
White Plains, NY 10607
xv111
-------
Dr. Jack Dean
Immunobiology Program and
Iiwunotoxlcology/Cell Biology program
CUT
P.O. Box 12137
Research Triangle Park, NC 27709
Dr. H. T. Delves
Chenlcal Pathology and Hunan
Metabollsn
Southampton General Hospital
Southampton S09 4XY
England
Dr. Fred deSerres
Assoc. Director for Genetics
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Robert Dixon
Laboratory of Reproductive and
Developmental Toxicology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Claire Ernhart
Department of Psychiatry
Cleveland Metropolitan General Hospital
Cleveland, OH 44109
Dr. Sergio Fachetti
Section Head - Isotope Analysis
Chemistry Division
Joint Research Center
121020 Ispra
Varese, Italy
Dr. Virgil Fen#
Department of Anatomy and Cytology
Dartmouth Medical School
Hanover, NH 03755
Dr. Alf F1schbe1n
Environmental Sciences Laboratory
Mt. Sinai School of Medicine
New York, NY 10029
Dr. Jack Fowle
Reproductive Effects Assessment Group
U.S. Environmental Protection Agency
RD-689
Washington, DC 20460
Dr. Bruce Fowler
Laboratory of Pharmacology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Warren Galke
Department of Blostatisties
and Epidemiology
School of Allied Health
East Carolina University
Greenville, NC 27834
Mr. Eric Goldstein
Natural Resources Defense
Council, Inc.
122 E. 42nd Street
New York, NY 10168
Dr. Harvey Gonlck
1033 Gayley Avenue
Suite 116
Los Angeles, CA 90024
Dr. Robert Goyer
Deputy Director
NIEHS
P.O. Box 12233
Dr. Stanley Gross
Hazard Evaluation Division
Toxicology Branch
U.S. Environmental Protection
Agency
Washington, DC 20460
Dr. Paul Hammond
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
Dr. Ronald D. Hood
Department of Biology
The University of Alabama
University, AL 35486
Dr. V. Houk
Centers for Disease Control
1600 Clifton Road, NE
Atlanta, GA 30333
xix
-------
Or. Loren D. toller
School of Veterinary Medicine
University of Idaho
Moscow. ID 83843
Dr. Kristal Kostial
Institute for Medical Research
ami Occupational Health
Yu-4l00 Zagreb
Yugoslavia
Or. Lawrence Kupper
Department of Biostatistics
UNC School of Public Health
Chapel Hill, HC 27514
Dr. Phillip Landrigan
Division of Surveillance,
Hazard Evaluation and Field Studies
Taft Laboratories - NIOSH
Cincinnati, OH 45226
Or. David Lawrence
Microbiology and Immunology Dept.
Albany Medical College of Union
University
Albany, NY 12208
Dr. Jane Lin-Fu
Office of Maternal and Child Health
Department of Health and Hunan Services
Rockvllle, MD 20857
Dr. Don Lynam
Air Conservation
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. Kathryn Mahaffey
Division of Nutrition
Food and Drug Adnlnistration
1090 Tusculun Avenue
Cincinnati, OH 45226
Dr. Ed McCabe
Department of Pediatrics
University of Wisconsin
Madison, WI 53706
Dr. Chuck Nauaan
Exposure Assessnent Group
U.S. Environmental Protection
Agency
Washington, DC 20460
Dr. Herbert L. Needleman
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Dr. H. Mitchell Perry
V.A. Medical Center
St. Louis, MO 63131
Dr. Jack Pierrard
E.I. duPont de Nemours and
Conpany, Inc.
Petroleum Laboratory
Wilmington, DE 19898
Dr. Sergio PioinelH
Columbia University Medical School
Division of Pediatric Hematology
and Oncology
New York, NY 10032
Dr. Magnus Piscator
Departnent of Environmental Hygiene
The Karolinska Institute 104 01
Stockholm
Sweden
Dr. - Robert Putna»
International Lead-Zinc
Research Organization
292 Madison Avenue
New York, NY 10017
Dr. Michael Rabinowitz
Children's Hospital Medical
Center
300 Longwood Avenue
Boston, MA 02115
XX
-------
Or. Harry Roels
Unite de Toxicol ogle
Industrlelle et Medicale
Universlte de Louvain
Brussels, Belgium
Dr. John Rosen
Division of Pediatric Metabolism
Albert Einstein College of Medicine
Montefiore Hospital and Medical Center
HI East 210 Street
Bronx, NY 10467
Dr. Michael Rutter
Department of Psychology
Institute of Psychiatry
OeCrtsplgny Park
London SE5 ML
England
Dr. Stephen R. Schroeder
Division for Disorders
of Development and Learning
Biological Sciences Research Center
University of North Carolina
Chapel Hill, NC 27514
Or. Anna-Maria Seppalainen
Institutes of Occupational Health
Tyoterveyslaltos
Haartmaninkatu 1
00290 Helsinki 29
Finland
Dr. Ellen Sllbergeld
Environmental Defense Fund
1525 18th Street, NW
Washington, DC 20036
Dr Ron Snee
E.I. duPont Nemours and
Company, inc.
Engineering Department L3167
Wilmington, DE 19898
Dr. Gary Ter Haar
Toxicology and Industrial
Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70S01
Mr. Ian von Lindern
Department of Chemical Engineering
University of Idaho
Moscow, Idaho 83843
Dr. Richard P. Wedeen
V. A. Medical Center
Tremont Avenue
East Orange, MJ 07019
xx1
-------
Chapter 10: Metabolism of Lead
Principal Author
Dr. Paul Mushak
Department of Pathology
School of Medicine
University of North Carolina
Chapel Hill, NC 27514
Contributing Author
Dr. Michael Rabinowltz
Children's Hospital Medical Center
300 Longwood Avenue
Boston, MA 02115
The following persons reviewed this chapter at EPA's request. The evaluations
and conclusions contained herein, however, are not necessarily those of the
reviewers?
Dr. Carol Angle
Department of Pediatrics
University of Nebraska
College of Medicine
Omaha, NE 68105
Dr. Lee Annest
Division of Health Examln. Statistics
National Center for Health Statistics
3700 East-West Highway
Hyattsville, MD 20782
Dr. Donald Barltrop
Department of Child Health
Westminister Children's Hospital
London SW1P 2NS
England
Dr. Irv Billick
Gas Research Institute
8600 West Bryn Mawr Avenue
Chicago, IL 60631
Dr. Joe Boone
Clinical Chemistry and
Toxicology Section
Centers for Disease Control
Atlanta, GA 30333
Dr. Robert Bornschein
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
Dr. A. C. Chamberlain
Environmental and Medical
Sciences Division
Atomic Energy Research
Estab11shaient
Harwell 0X11
England
Dr. Neil Chernoff
Division of Developnental Biology
M0-67
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Julian Chisolm
Baltimore City Hospital
4940 Eastern Avenue
Baltimore, MD 21224
Mr. Jerry Cole
International Lead-Z1nc Research
Organization
292 Madison Avenue
New York, NY 10017
xxii
-------
Dr. Max Costa
Department of Pharmacology
University of Texas Medical School
Houston, TX 77025
Or. Anita Curran
Commissioner of Health
Westchester County
White Plains, NY 10607
Dr. Jack Dean
Immunoblology Program and
Immunotoxicology/Cel1 Biology program
CUT
P.O. Box 12137
Research Triangle Park, NC 27709
Dr. H.T. Delves
Chemical Pathology and Hunan Metabolism
Southampton General Hospital
Southampton S09 4XY
England
Dr. Fred deSerres
Assoc. Director for Genetics
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Or. Robert Dixon
Laboratory of Reproductive and
Developmental Toxicology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Claire Ernhart
Department of Psychiatry
Cleveland Metropolitan General Hospital
Cleveland, OH 44109
Or. Sergio Fachettl
Section Head - Isotope Analysis
Chemistry 01vision
Joint Research Center
121020 Ispra
Varese, Italy
Dr. Virgil Fern
Department of Anatoay and Cytology
Dartmouth Medical School
Hanover, NH 03755
Dr. Alf Fischbein
Environmental Sciences Laboratory
Mt. Sinai School of Medicine
New York, NY 10029
Dr. Dr. Jack Fowle
Reproductive Effects Assessment
Group
U.S. Environmental Protection
Agency
RD-689
Washington, 0C 20460
Or. Bruce Fowler
Laboratory of Pharmacology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Warren Galke
Department of Biostatisties
and Epidemiology
School of Allied Health
East Carolina University
Greenville, NC 27834
Mr. Eric Goldstein
Natural Resources Defense
Council, Inc.
122 E. 42nd Street
New York, NY 10168
Dr. Harvey Gonick
1033 Gayley Avenue
Suite 116
Los Angeles, CA 90024
Dr. Robert Goyer
Deputy Director
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Or. Stanley Gross
Hazard Evaluation Division
Toxicology Branch
U.S. Environmental Protection
Washington, DC 20460
Dr. Paul Hamond
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
-------
Dr. Ronald D. Hood
Department of Biology
The University of Alabana
University, AL 35486
Dr. V. Houk
Centers for Disease Control
1600 Clifton Road, HE
Atlanta, GA 30333
Or. Loren 0. Roller
School of Veterinary Medicine
University of Idaho
Moscow, ID 83843
Dr. Kristal Kostial
Institute for Medical Research
and Occupational Health
Yu-4100 Zagreb
Yugoslavia
Or, Lawrence Kupper
Departnent of 81ostatisties
UNC School of Public Health
Chapel Hill, NC 27514
Dr. Phillip Landrigan
Division of Surveillance,
Hazard Evaluation and Field Studies
Taft Laboratories - NIOSH
Cincinnati, OH 45226
Or. David Lawrence
Microbiology and Immunology Dept.
Albany Medical College of Union
University
Albany, NY 12208
Dr. Jane lin-Fu
Office of Maternal and Child Health
Department of Health and Human Services
Rockville, MO 20857
Or. Don Lynaa
Air Conservation
Ethyl Corporation
411 Florida Boulevard
Baton Rouge, LA 70801
Dr. Kathryn Mahaffey
Division of Nutrition
Food and Drug Administration
1090 Tusculum Avenue
Cincinnati, OH 45226
1 xxiv
Dr. Ed McCabe
Department of Pediatrics
University of Wisconsin
Madison, WI 53706
Or. Chuck Nauman
Exposure Assessment Group
U.S. Environmental Protection Agency
Washington, DC 20460
Or. Herbert L. Neddlenan
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Or. H. Mitchell Perry
V,A. Medical Center
St. Louis, MO 63131
Dr. Jack Pierrard
E.I. duPont de Nemours and
Company, Inc.
Petroleum Laboratory
Wilmington, DE 19898
Dr. Sergio Piomelli
Columbia University Medical School
Division of Pediatric Hematology
and Oncology
New York, NY 10032
Or. Magnus Plscator
Department of Environmental Hygiene
The Karolinska Institute 104 01
Stockholm
Sweden
Or. Robert Putnam
International Lead-Zinc
Research Organization
292 Madison Avenue
New York, NY 10017
Or. Harry Roels
Unite de Toxicologle
Industrielle et Medicale
Universite de Louvain
Brussels, Belgium
Dr. John Rosen
Division of Pediatric Metabolism
Albert Einstein College of Medicine
Montefiore Hospital and Medical Center
111 East 210 Street
Bronx, NY 10467
-------
Dr. Michael Rutter
Department of Psychology
Institute of Psychiatry
DeCrespigny Park
London SE5 SAL
England
Dr. Stephen R. Schroeder
Division for Disorders
of Development and Learning
Biological Sciences Research Center
University of North Carolina
Chapel Hill, NC 27514
Dr. Anna-Maria Seppalainen
Institutes of Occupational Health
Tyoterveyslaltos
Haartmaninkatu 1
00290 Helsinki 29
Finland
Dr. Ellen Sllbergeld
Environmental Defense Fund
1525 18th Street, NW
Washington, DC 20036
Dr. Ron Snee
E.I. duPont Nemours and
Company, Inc.
Engineering Department L3167
Wilmington, OE 19898
Dr. Gary Ter Haar
Toxicology and Industrial
Hygiene
Ethyl Corporation
451 Florida Boulevard
Mr. Ian von Lindern
Department of Chemical
Engineering
University of Idaho
Moscow, ID 83843
Dr. Richard P. Wedeen
V.A. Medical Center
Tremont Avenue
East Orange, NJ 07019
xxv
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Chapter 11: Assessment of Lead Exposures and Absorption 1n Human Populations
Principal Authors
Dr. Warren Galke
Department of Biostatlsties and Epidemiology
School of Allied Health
East Carolina University
Greenville, NC 27834
Dr. Vic Hasselblad
Biometry Division
MD-55
U.S. Environmental Protection
Agency
Research Triangle Park, NC 27711
Dr. Alan Marcus
Department of Mathematics
Washington State University
Pullman, Washington 99164-2930
Contributing Author:
Dr. Dennis Kotchmar
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
The following persons reviewed this chapter at EPA's request. The evaluations
and conclusions contained herein, however, are not necessarily those of the
reviewers. •
Dr. Carol Angle
Department of Pediatrics
University of Nebraska
College of Medicine
Omaha, NE 68105
Dr. Lee Annest
Division of Health Examin. Statistics
National Center for Health Statistics
3700 East-West Highway
Hyattsvllle, MD 20782
Dr. Donald Barltrop
Department of Child Health
Westminister Children's Hospital
London SW1P 2NS
England*
Dr. Irv Billick
Gas Research Institute
8600 West Bryn Hawr Avenue
Chicago, IL 60631
Dr. Joe Boone
Clinical Chemistry and
Toxicology Section
Centers for Disease Control
Atlanta, GA 30333
Dr. Robert Bornschein
University of Cincinnati
Kettering Laboratory
Cincinnati, OH 45267
Dr. A. C. Chamberlain
Environmental and Medical
Sciences Division
Atomic Energy Research
Establishment
Harwell 0X11
England
Dr. Neil Chemoff
Division of Developmental Biology
MD-67
U.S. Environmental Protection
Agnecy
Research Triangle Park, NC 27711
xxvi
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Of. Julian Chisolm
Baltimore City Hospital
4940 Eastern Avenue
Baltimore, MD 21224
Mr. Jerry Cole
International Lead-Z1nc Research Organization
292 Madison Avenue
New York, NY 10017
Or. Max Costa
Department of Pharmacology
University of Texas Medical School
Houston, TX 77025
Or. Anita Curran
Commissioner of Health
Westchester County
White Plains, NY 10S07
Dr. Jack Dean
Immunobiology Program and
Ionunotoxlcology/Cell Biology Program
CUT
P.O. Box 12137
Research Triangle Park, NC 27709
Or. Fred deSerres
Assoc. Director for Genetics
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Or. Robert Dixon
Laboratory of Reproductive and
Developmental Toxicology
NIEHS
P.O. Box 12233
Research TH angle Park, NC 27709
Dr. Claire Ernhart
Department of Psychiatry
Cleveland Metropolitan General Hospital
Cleveland, OH 44109
Dr. Sergio Fachetti
Section Head - Isotope Analysis
Chemistry Division
Joint Research Center
121020 Ispra
Varese, Italy
Dr. Virgil Fern
Department of Anatomy and Cytology
Dartmouth Medical School
Hanover, NH 03755
Dr. Alf Fischtoein
Environmental Sciences Laboratory
Mt. Sinai School of Medicine
New York, NY 10029
Dr. Jack Fowle
Reproductive Effects Assessment
Group
U.S. Environmental Protection
Agency
RO-689
Washington, DC 20460
Dr. Bruce Fowler
laboratory of Pharmocology
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Mr. Eric Goldstein
Natural Resources Defense
Council, Inc.
School of Allied Health
122 E. 42nd Street
New York, NY 10168
Dr. Harvey Gonick
1033 Gayley Avenue
Suite 116
Los Angeles, CA 90024
Or. Robert Goyer
Oeputy Director
NIEHS
P.O. Box 12233
Research Triangle Park, NC 27709
Dr. Stanley Gross
Hazard Evaluation Division
Toxicology Branch
U.S. Environmental Protection
Dr. Paul Hammond
University of Cincinnati
Kettering Laboratory
3223 Eden Avenue
Cincinnati, OH 45267
xxvii
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Dr. Ronald 0. Hood
Department of Biology
The University of Alabama
University, AL 35486
Dr. V. Houk
Centers for Disease Control
1600 Clifton Road, NE
Atlanta, GA 30333
Dr. Loren Koller
School of Veterinary Medicine
University of Idaho
Moscow, ID 83843
Or. Kristal Kostial
Institute for Medical Research
and Occupational Health
Yu-4100 Zagreb
Yugoslavia
Dr. Lawrence Kupper
Department of Biostatistics
UNC School nf Public Health
Chapel H111, NC 27514
Or. Phillip Landrigan
Division of Surveillance,
Hazard Evaluation and Field Studies
Taft Laboratories - NIOSH
Cincinnati, OH 45226
Dr. David Lawrence
Microbiology and Immunology Dept.
Albany Medical College of Union
University
Albany, NY 12208
Dr. Jane Lln-Fu
Office of Maternal and Child Health
Department of Health and Human Services
Rockvllle, M0 20857
Dr. Don Lynam
Air Conservation
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Dr. Kathryn Mahaffey
Division of Nutrition
Food and Drug Administration
1090 Tusculum Avenue
Cincinnati, OH 45226
Dr. Ed McCabe
Department of Pediatrics
University of Wisconsin
Madison, WI 53706
Or. Paul Mushak
Department of Pathology
UNC School of Medicine
Chapel Hill, NC 27514
Dr. Chuck Nauman
Exposure Assessment Group
U.S. Environmental Protection
Agency
Washington, 0C 20460
Dr. Herbert I. Needleman
Children's Hospital of Pittsburgh
Pittsburgh, PA 15213
Dr. H. Mitchell Perry
V.A. Medical Center
St. Louis, M0 63131
Dr. Jack Pierrard
E.I. duPoint de Nemours and
Company, Inc.
Petroleum Laboratory
Wilmington, DE 19898
Dr. Sergio PiomelH
Columbia University Medical School
Division of Pediatric Hematology
and Oncology
New York, NY 10032
Dr. Magnus Piscator
Department of Environmental Hygiene
The Karollnska Institute 104 01
Stockholm
Sweden
xxvlii
-------
Dr. Robert Pulnam
International Lead-Zinc
Research Organization
292 Madison Avenue
New York, NY 10017
Dr. Michael Rabinowitz
Children's Hospital Medical Center
300 Longwood Avenue
Boston, MA 02115
Dr. Harry RoeIs
Unite de Toxicologie
Industrie!le et Medicate
Universite de Louvain
Brussels, Belgium
Dr. John Rosen
Division of Pediatric Metabolism
Albert Einstein College of Medicine
Montefiore Hospital and Medical Center
111 East 210 Street
Bronx, NY 10467
Dr. Stephen R. Schroeder
Division for Disorders
of Development and Learning
Biological Sciences Research Center
University of North Carolina
Chapel Hill, NC 27S14
Dr. Anna-Maria Seppalainen
Institutes of Occupational Health
Tyoterveyslaitos
Haartmaninkatu 1
00290 Helsinki 29
Finland
Dr. Ellen Silbergeld
Environmental Defense Fund
1525 18th Street, NV
Washington, DC 20036
Dr. Ron Snee
E.I. duPont Nemours and
Company, Inc.
Engineering Department L3267
Wilmington, DE 19898
Dr. Gary Ter Haar
Toxicology and Industrial
Hygiene
Ethyl Corporation
451 Florida Boulevard
Baton Rouge, LA 70801
Mr. Ivon von Lindern
Department of Chemical Engineering
University of Idaho
Moscow, ID 83843
Dr. Richard P. Weeden
V.A. Medical Center
Tremont Avenue
East Orange, NJ 07019
xxix
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PRELIMINARY DRAFT
9, QUANTITATIVE EVALUATION OF LEAD AND BIOCHEMICAL INDICES
OF LEAD EXPOSURE IN PHYSIOLOGICAL MEDIA
9.1 INTRODUCTION
In order to completely understand a given agent's effects on an organism, e.g., dose-
effect relationships, a quantitative evaluation of the substance in some indicator medium and
knowledge of the physiological parameters associated with exposure is vital. This said, two
questions follow:
1) What are the most accurate, precise, and efficient ways to
carry out such measurements?
2) In the case of lead (lead itself or biological indicators),
which measurement methods in which media are most appropri-
ate for each particular exposure?
Under the rubric of "analysis" are a number of discrete steps, all of which are important
contributors to the quality of the final result: (1) collection of samples and transmission
to the laboratory; (2) laboratory manipulation of samples, physically and chemically, before
analysis by instruments; (3) instrumental analysis and quantitative measurement; and (4)
establishment of relevant criteria for accuracy and precision, namely, internal and external
quality assurance checks. Each of these steps is discussed in this chapter.
It is clear that the definition of "satisfactory analytical method" for lead has been
changing over the years in ways paralleling (1) the evolution of more sophisticated instrumen-
tation and procedures, (2) a greater awareness of such factors as background contamination and
loss of element from samples, and (3) development of new statistical methods to analyze data.
For example, current methods of lead analysis, such as anodic stripping voltammetry, back-
ground-corrected atomic absorption spectrometry, and isotope dilution mass spectrometry (par-
ticularly the latter), are more sensitive and specific than the older classical approaches.
Increasing use of the newer methods would tend to result in lower lead values being reported
for a given sample. Whether this trend In analytical improvement can be isolated from such
other variables as temporal changes in exposure is another matter.
Since lead Is ubiquitously distributed as a contaminant, the constraints (i.e., ultra-
clean, ultra-trace analysis) placed upon a laboratory attempting analysis of geochenical
samples of pristine origin, or of extremely low lead levels in biological samples such as
plasma, are quite severe. Very few laboratories can credibly claim such capability. Ideally,
similar standards of quality should be adhered to across the rest of the analytical spectrum.
With many clinical, epidemiological, and experimental studies, however, this may be unrealis-
tic, given practical limitations and objectives of the studies. Laboratory performance is but
23PBI2/C 9-1 7/1/83
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PRELIMINARY DRAFT
one part of the quality equation; the problems of sampling are equally Important but less sub-
ject to tight control. The necessity of rapidly obtaining a blood sample In cases of suspec-
ted lead poisoning, or of collecting hundreds or thousands of blood samples 1n urban popu-
lations, limits the number of sampling safeguards to those that can be realistically achieved.
Sampling in this context will always be accompanied by a certain amount of analytical
"suspicion." Furthermore, a certain amount of biological lead analysis data is employed for
comparative purposes, as In experimental studies concerned with the relative Increase in tis-
sue burden of lead associated with increases in doses or severity of effects- In addition,
any major compromise of an analytical protocol may be statistically discernible. Thus, anal-
ysis of biological media for lead must be done under protocols that minimize the risk of In-
accuracy. Specific accuracy and precision characteristics of a method in a particular report
should be noted to permit some judgment on the part of the reader about the influence of
methodology on the reported results.
The choice of measurement method (see Question 2) and medium for analysis is dictated
both by the type of information desired and by technical or logistical considerations. As
noted elsewhere 1n this document, whole blood lead reflects recent or continuing exposure,
whereas lead 1n mineralized tissue, such as deciduous teeth, reflects an exposure period of
months and years. While urine lead values are not particularly good correlates of lead ex-
posure under steady-state conditions in populations at large, such measurements may be of con-
siderable clinical value. In acquisition of blood samples, the choice of venipuncture or
finger puncture will be governed by such factors as cost and feasibility, contamination risk,
the biological quality of the sample, etc. The use of biological indicators that strongly
correlate with lead burden may be more desirable since they provide evidence of actual re-
sponse and, together with blood lead data, provide a less risky diagnostic tool for assessment
of lead exposure.
9.2 DETERMINATIONS OF LEAD IN BIOLOGICAL MEDIA
9.2.1 Sampling and Sample Handling Procedures for Lead 1n Biological Media
Lead analysis in biological media requires careful collection and handling of samples for
two special reasons: (1) lead occurs at trace levels In most Indicators of subject exposure,
even under conditions of high lead exposure, and (2) such samples must be obtained against a
backdrop of pervasive contamination, the full extent of which may still be unrecognized by
many laboratories.
The reports of Speecke et al. (1976), Patterson and Settle (1976), Murphy (1976), Berman
(1976), and Settle and Patterson (1980) review detailed aspects of the problems of sampling
and subsequent sample handling in the laboratory. It is clear from these discussions that the
23PB12/C 9-2 7/1/83
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PRELIMINARY DRAFT
normal precautions taken In the course of sample acquisition (detailed below for clinical and
epidemiological studies) should not be taken as absolute, but rather as what is practical and
feasible. Furthermore, it nay also be the case that the inherent sensitivity or accuracy of a
given methodology or instrumentation is less of a determining factor in the overall analysis
than is quality of sample collection and handling.
9.2.1.1 Blood Sampling. Samples for blood lead determination may be collected by venipunc-
ture (venous blood) or finger tip puncture (capillary blood). Collection of capillary vs.
venous blood is normally decided by a number of factors, including the feasibility of obtain-
ing samples during screening of many subjects and the difficulty of securing subject compli-
ance, particularly in the case of children and their parent's. Furthermore, capillary blood
may be collected as discrete quantities in small-volume capillary tubes or as spots on filter
paper disks. With capillary tubes, obtaining good mixing with anticoagulant to avoid clotting
is important, as is the problem of lead contamination of the tube. The use of filter paper
requires the selection of paper with uniform composition, low lead content, and uniform blood
dispersal, characteristics.
Whether venous or capillary blood is collected, much care must be exercised in cleaning
the site before puncture as well as in selecting lead-free receiving containers. Cooke et al.
(1974) employed vigorous scrubbing with a low-lead soap solution and deionized water rinsing,
while Marcus et al. (1975) carried out preliminary cleaning with an ethanolic citric acid
solution followed by 70 percent ethanol rinsing. The vigor in cleaning the puncture site Is
probably as important as any particular choice of cleaning agent. Marcus et al. (1977) noted
that in one procedure for puncture site preparation, where the site Is covered with wet paper
towels, contamination will occur if the paper towels are made from recycled paper, owing to
significant lead retention 1n recycled paper.
In theory, capillary and venous blood lead levels should be virtually Identical, although
the available literature indicates that some differences, which mainly reflect problems of
sampling, do arise in the case of capillary blood. A given amount of contaminant has a
greater impact on a 100 jj! fingerstlck sample than on a 5 ml sample of venous blood. Finger
coating techniques may reduce some of the contamination problem (Mitchell et al., 1974). An
additional problem is the presence of lead in the anticoagulants used to coat capillary tubes.
Also, lower values of capillary vs. venous blood lead may reflect "dilution" of the sample by
extracellular fluid owing to excessive compression of the puncture site. When Joselow and
Bogden (1972) compared a method using finger puncture and spotting onto filter paper with a
procedure using venous blood and Hessel's procedure (1968) for flame atomic absorption spec-
trometry, they obtained a correlation coefficient of r = 0.9 (range, 20-46 pg/dl). Similarly,
Cooke et al. (1974) found an r value of 0.8 (no range given), while Mitchell et al. (1974)
23PB12/C
9-3
7/1/83
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PRELIMINARY DRAFT
obtained a value of 0.92 (10-92 |jg/dl). Mahaffey et al. (1979) found that capillary blood
levels in a comparison test were approximately 20 percent higher than corresponding venous
blood levels in the sane subjects, presumably reflecting sample contamination. Similar eleva-
tions have been described by DeSilva and Donnan (1980). Carter (1978) has found that blood
samples with lower hemoglobin levels may spread onto filter paper differently from normal
hemoglobin samples, requiring correction in quantification to obtain values that are reliable.
This complication should be kept in mind when considering children, who are frequently prone
to iron-deficiency anemia.
The relative freedom of the blood container from interior surface lead and the amount of
lead in the anticoagulant used are important considerations in venous sampling. For studies
focused on "normal" ranges, such tubes may add some lead to blood and still meet certification
requirements. The "low-lead" heparinized blood tubes commercially available (blue stopper
Vacutainer, Becton-Oickinson) were found to contribute less than 0.2 pg/dl to whole blood
samples (Rabinowitz and Needleman, 1982). Nackowski et al. (1977) surveyed a large variety of
commercially available blood tubes for lead and other metal contamination. Lead uptake by
blood over time from the various tubes was minimal with the "low-lead" Vacutainer tubes and
with all but four of the other tube types. In the large survey of Mahaffey et al. (1979),
5-ml Monoject (Sherwood) or 7-ml lavender-top Vacutainer (Becton-D1ck1nson) tubes were found
satisfactory. However, when more precision 1s needed, tubes are best recleaned in the labor-
atory and lead-free anticoagulant added (although this would be less convenient for sampling
efficiency than the commercial tubes). In addition, blank levels for every batch of samples
should be verified.
9.2.1.2 Urine Sampling. Urine samples require collection in lead-free containers and caps as
well as the addition of a low-lead bactericide if samples are to be stored for any period of
time. While not always feasible, 24-hour samples should be obtained, as such collection would
level out any effect of variation in excretion over time. If spot sampling is done, lead
levels should be expressed per unit creatinine. For 24-hour collections, corrections must be
made for urine density.
9.2.1.3 Hair Sampling. The usefulness of hair lead analysis depends on the manner of samp-
ling. Hair samples should be removed from subjects by some consistent method, either by a
predetermined length measured from the skin or by using the entire hair. Hair should be
placed In air-tight containers for shipment or storage. For segmental analysis, the entire
hair length is required.
9.2.1.4 Mineralized Tissue. An important consideration in deciduous tooth collection is
consistency in the type of teeth collected from various subjects. Fosse and Justesen (1978)
reported no difference in lead content between molars and incisors, and Cbatman and Wilson
(1975) reported comparable whole tooth levels for cuspids, incisors, and molars. On the other
hand, Mackie et al. (1977) and Lockeretz (1975) noted levels varying with tooth type, with a
23PB12/C 9-4 7/1/83
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PRELIMINARY DRAFT
statistically significant difference (Mackle et al., 1977) between second molar (lowest
levels) and incisors (highest levels). The fact that the former two studies found rather low
overall lead levels across groups, while Mackle et al. (1977) reported higher values, suggests
that dentition differences 1n lead content may be magnified at relatively higher levels of ex-
posure. Delves et al. (1982), comparing pairs of central Incisors or pairs of central and
lateral Incisors from the same child, found that lead levels may even vary within a specific
type of tooth. These data suggest the desirability of acquiring two teeth per subject to get
an average lead value.
Teeth containing fillings or extensive decay are best eliminated from analysis. Mackie
et al. (1977) discarded decayed teeth if the extent of decay exceeded approximately 30 per-
cent.
9.2.1.5 Sample Handling in the Laboratory. With blood samples, there is the potential prob-
lem of the effect of storage on the lead content. It is clear that dilute aqueous solutions
of lead will surrender a sizable portion of the lead content to the container surface, whether
glass or plastic (Issaq and Zielinski, 1974; Unger and Green, 1977); whether there 1s a com-
parable effect, or the extent of such an effect, with blood 1s not clear. Unger and Green
(1977) claim that lead loss from blood to containers parallels that seen with aqueous solu-
tions, but their data do not support this assertion. Moore and Meredith (1977) used isotopic
lead spiking (203Pb) with and without carrier in various containers at differing temperatures
to monitor lead stability in blood over time. The only material loss occurred with soda glass
at room temperature after 16 days. Nackowski et al, (1977) found that "low-lead" blood tubes,
while quite satisfactory in terms of sample contamination, began to show transfer of lead to
the container wall after four days. Meranger et al. (1981) studied movement of lead, spiked
to various levels, to containers of various composition as a function of temperature and time.
In all cases, reported lead loss to containers was significant. However, there are problems
with the above reports. Spiked samples probably are not incorporated Into the same biochemi-
cal environment as lead inserted In vivo. The Nackowski et al. (1977) stutfy did not indicate
whether the blood samples were kept frozen or refrigerated between testing intervals.
Mitchell et al. (1972) found that the effect of blood storage depends on the method of anal-
ysis, with lower recoveries of lead from aged blood being seen using the Hessel (1968) method.
Lerner (1975) collected blood samples (35 originally) from a single subject into lead-
free tubes and, after freezing, forwarded them in blind fashion to a certified testing labor-
atory over a period of 9 months. Four samples were lost, while one was rejected as being
grossly contaminated (4 standard deviations from mean). Of the remaining 30 samples, the mean
was 18.3 Mfl/dl with a standard deviation (S.D.) of 3.9. The analytical method had a precision
of ±3.5 MO Pb/dl (1 = S.D.) at normal levels of lead, suggesting that the overall stability of
the samples in terms of lead content was good. Boone et al. (1979), reported that samples
23PB12/C 9-5 7/1/83
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PRELIMINARY DRAFT
frozen for periods of less than a year showed no effect of storage, while Piscator (1982)
noted no change in low levels {<10 Mg/dl) when samples were stored at -20°C for 6 Months.
Based on the above data, it appears that blood samples to be stored for any period of time
should be frozen rather than refrigerated, with care taken to prevent breaking of the tube
during freezing. Teeth and hair samples, when stored in containers to minimize contamination,
are indefinitely stable.
The actual site of analysis should be as lead-free as possible. Given the uncommon
availability of an "ultra-clean" facility such as that described by Patterson and Settle
(1976), the next desirable level of laboratory cleanliness 1s the "Class 100" facility, in
which there are fewer than 100 airborne particles >0.5 pm. These facilities employ high ef-
ficiency particulate air filtering and laminar air flow (with movement away from sample
handling areas). Totally inert surfaces in the working area and an antechamber for removing
contaminated clothes, appliance cleaning, etc. are other necessary features.
All plastic and glass ware coning into contact with samples should be rigorously cleaned
and stored away from dust contact; materials such as ashing vessels should permit minimal lead
leaching. In this regard, Teflon and quartz ware is more desirable than other plastics or
borosilIcate glass (Patterson and Settle, 1976).
Reagents, particularly for chemical degradation of biological samples, should be both
certified and periodically tested for retention of quality. Several commercial grades of re-
agents are available, although precise work may require doubly purified materials from the
National Bureau of Standards. These reagents should be stored with a minimum of surface con-
tamination around the top of the containers.
For a more detailed discussion of appropriate laboratory practices, the reader may con-
sult LaFleur (1976).
9.2.2 Methods of Lead Analysis
Detailed technical discussion of the array of instruments available to measure lead in
blood and other media is outside the scope of this Chapter (see Chapter 4). This discussion
is structured more appropriately to those aspects of methodology dealing with relative sensi-
tivity, specificity, accuracy and precision. While there is increasing acceptance of interna-
tional standardized units (SI units) for expressing lead levels in various media, units famil-
iar to clinicians and epidemiologists will be used here. (To convert pg Pb/dl blood to SI
units (pmoles/Hter), multiply by 0.048.)
Many reports over the years have purported to offer satisfactory analysis of lead in bio-
logical media, but 1n fact have shown rather meager adherence to criteria for accuracy and
precision or have shown a lack of demonstrable utility across a wide spectrum of analytical
applications. Therefore, discussion in this section is confined to "definitive" and reference
23PB12/C 9-6 7/1/83
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PRELIMINARY DRAFT
Methods for lead analysts, except for a brief treatment of the traditional but now widely sup-
planted col orimetric method.
Using the definition of Call and Reed (1976), a definitive method is one in which all
major or significant parameters are related by solid evidence to the absolute mass of the ele-
ment with a high degree of confidence. A reference method, by contrast, 1s one of demonstra-
ted accuracy, validated by a definitive method and arrived at by consensus through performance
testing by a number of different laboratories. In the case of lead 1n biological media, the
definitive method is isotope-dilution mass spectrometry (IDMS). IDMS accuracy conies from the
fact that all manipulations are on a weight basis Involving simple procedures.. The measure-
ments entail only ratios and not the absolute determinations of the isotopes involved, which
greatly reduces Instrumental corrections or errors. Reproducible results to a precision of
one part In 104 or 10s are routine with specially designed instruments.
In terms of reference methods for lead in biological media, such a label cannot techni-
cally be attached to atomic absorption spectrometry in Its various instrumentation/
methodology configurations or to the electrochemical technique, anodic stripping voltametry.
However, these have been termed reference methods insofar as their precision and accuracy can
be verified or calibrated against IDMS.
Other methods that are recognized for trace metal analysis in general are not fully ap-
plicable to biological lead or have Inherent shortcomings. X-ray fluorescence analysis lacks
the requisite sensitivity for media with low lead content and the associated sample prepara-
tion may present a high contamination risk. A notable exception may be X-ray fluorescence
analysis of teeth or bone in situ as discussed below. Neutron activation analysis is the
method of choice with many elements, but is not technically feasible for lead analysis because
of the absence of long-lived isotopes.
9.2.2.1 Lead Analysis In Whole Blood. The first generally accepted technique for quantifying
lead in whole blood and other biological media was a colorimetric method that involved spec-
trophotometry measurement based on the binding of lead to a chromogenlc agent to yield a
chromophoHc complex. The complexing agent has typically been dithlzone, 1,5-dlphenylthio-
carbazone, yielding a lead complex that is spectrally measured at 510 nm.
Two variations of the spectrophotometric technique used when measuring low levels of lead
have been the USPHS (National Academy of Sciences, 1972) and APHA (American Public Health
Association, 1955) procedures. In both, venous blood or urine is wet ashed using concentrated
nitric acid of low lead content followed by adjustment of the ash with hydroxy!amine and so-
dium citrate to a pH of 9-10. Cyanide ion is added and the solution extracted with dithlzone
in chloroform. Back extraction removes the lead Into dilute nitric acid; the acid l«*yer 1s
treated with ammonia, then cyanide, and re-extracted with dithlzone In chloroform. The
extracts are read in a spectrophotometer at 510 nm. Bismuth interference is handled (APHA
23PB12/C 9-7 7/1/83
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PRELIMINARY DRAFT
variation) by removal with dlthlzone at pH 3.4. According to Lerner (1975), the analytical
precision in the "normal" range is about ±3.5 pg Pb/dl (1 = S.D.), using 5 ml of sample.
The most accurate and precise method for lead measurement in blood is isotope dilution
mass spectrometry. As typified by the report of Machlan et al. (1976), whole blood samples
are accurately weighed, and a weighed aliquot of 206Pb-enriched isotope solution 1s added.
After sample decomposition with ultra-pure nitric and perchloric acids, samples are evapo-
rated, residues are taken up in dilute lead-free hydrochloric acid, and lead is isolated using
anlon-exchange columns. Column eluates are evaporated with the above acids, and lead 1s
deposited onto high purity platinum wire from dilute perchloric acid. The 206Pb/208Pb ratio
1s then determined by thermal Ionization mass spectrometry. Samples without added isotope and
reagent blanks are also carried through the procedure. In terms of precision, the 95 percent
confidence level for lead samples overall 1s within 0.15 percent. Due to the expense Incurred
by the requirements for operator expertise, the amount of time Involved, and the high standard
of laboratory cleanliness, IDMS Is mainly of practical value 1n the development of standard
reference materials and for the verification of other analytical methods.
Atomic absorption spectrometry (AAS) is widely used for lead measurements in whole blood,
with sample analysis involving analysis of venous blood with chemical degradation, analysis of
liquid samples with or without degradation, and samples applied to filter paper. It is thus
the most flexible for samples already collected or subject to manipulation.
By means of a flame or electrothermal excitation, ionic lead in some matrix is first vapor-
ized and then converted to the atomic state, followed by resonance absorption from either a
hollow cathode or electrodeless discharge lamp generating lead absorption lines at 217.0 and
283.3 nm. After monochrometer separation and photomultiplier enhancement of the differential
signal, it is measured electronically.
The earliest methods of atomic absorption spectrometric analysis involved the aspiration
Into a flame of ashed samples of blood, usually subsequent to extraction Into an organic sol-
vent to enhance sensitivity by preconcentration. Some methods did not involve digestion steps
prior to solvent extraction (Kopito et al., 1974). Of these various flame AAS methods, that
of Hessel's (1968) technique continues to be used with some frequency.
Currently, lead measurement in blood by AAS employs several different methods that permit
greater sensitivity, precision, and econon^y of sample and time. The flame method of Delves
(1970), called the "Delves cup" procedure, usually Involves delivery of discrete small samples
(£100 pi) of unmodified whole blood to nickel cups, with subsequent drying and peroxide decom-
position of organic content before positioning 1n the flame. The marked enhancement of sen-
sitivity over conventional flame aspiration 1s due to Immediate, total consumption of the
sample and the generation of a localized population of atoms. In addition to discrete blood
volumes, blood-containing filter paper disks have been used (Joselow and Bogden, 1972; Cernll
23PB12/C 9-8 7/1/83
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PRELIMINARY DRAFT
and Sayers, 1971; Plomilli et al., 1980). Several modifications of the Delves method include
that of Edlger and Coleman (1972), 1n which dried blood samples in the cups are pre-ign1ted to
destroy organic matter by placement near the flame in a precise, repeatable manner, and the
variation of Barthel et al. (1973), in which blood samples are mixed with dilute nitric acid
in the cups followed by drying in an oven at 200°C and charring at 450°C on a hot plate. A
number of laboratories eschew even these modifications and follow dispensing and drying with
direct placement of the cup Into the flame (e.g., Mitchell et al., 1974). The Delves cup pro-
cedure may require correction for background spectral interference, which is usually achieved
by instrumentation equipped at a non-resonance absorption line. While the 217.0 ran line of
lead is less subject to such Interference, precise work is best done with correction. This
method as applied to whole blood lead appears to have an operational sensitivity down to 1.0
Mg Pb/dl, or somewhat below when competently employed, and a relative precision of approxi-
mately 5 percent in the range of levels encountered in the United States.
AAS methods using electrothermal (furnace) excitation in lieu of a flame can be approxi-
mately 10-fold more sensitive than the Delves procedure. A number of reports describing whole
blood lead analysis have appeared in the literature (Lawrence, 1982, 1983). Because of In-
creased sensitivity, the "flameless" AAS technique permits the use of small blood volumes
(1-5 pi) with samples undergoing drying and dry ashing |n situ. Physicochemical and spectral
interferences are inherently severe with this approach, requiring careful background cor-
rection. In one flameless AAS configuration, background correction exploits the Zeeman
effect, where correction is made at the specific absorption line of the element and not over a
band-pass region, as 1s the case with the deuterium arc. While control of background Inter-
ference up to 1.5 molecular absorbence is claimed with the Zeeman system (Koizumi and Yasuda,
1976), it is technically preferable to employ charring before atomlzation. Hinderberger et
al. (1981) used dilute ammonium phosphate solution to minimize chemical interference in their
furnace AAS method.
Precision can be a problem 1n the flameless technique unless careful attention 1s paid to
the problem of sample dlffuslbillty over and Into the graphite matrix of the receiving recep-
tacle -- tube, cup, or rod. With the use of diluted samples and larger applied volumes, the
relative precision of this method can approach that of the Delves technique (Delves, 1977).
In addition to the various atomic absorption spectral methods noted above, electro-
chemical techniques have been applied to blood lead analysis. Electrochemical methods, in
theory, differ from AAS methods in that the latter are "concentration" methods regardless of
sample volumes available, while electrochemical analysis involves bulk consumption of sample
and hence would have Infinite sensitivity, given an infinite sample volume. This intrinsic
property is of little practical advantage given usual sample volume, instrumentation design,
and blank limits.
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PRELIMINARY DRAFT
The most widely used electrochemical method for lead measurement in whole blood and other
biological media is anodic stripping voltammetry (ASV) which is also probably the most sensi-
tive, as it involves an electrochemical preconcentration (deposition) stfep in the analysis
(Matson and Roe, 1966; Matson et al., 1970). In this method, samples such as whole blood
(50-100 jil), are preferably but not commonly wet ashed and reconstituted in dilute add or
made electro-available with metal exchange reagents. Using freshly prepared composite elec-
trodes of mercury film deposited on carbon, lead is plated out from the solution for a speci-
fic amount of time and at a selected negative voltage. The plated lead is then reoxldlzed in
the course of anodic sweeping, generating a current peak that m^y be recorded on a chart or
displayed on commercial instruments as units of concentration (pg/dl).
One alternative to the time and space demands of wet ashing blood samples is the use of
metal exchange reagents that displace lead from binding sites in blood by competitive binding
(Morell and Giridhar, 1976; Lee and Meranger, 1980). In one commercial preparation, this re-
agent consists of a solution of calcium, chromium, and mercuric ions. Use of the metal ex-
change reagent adds a chemical step that must be carefully controlled for full recovery of
lead from the sample.
The working detection limit of ASV for blood is comparable to that of the AAS flameless
methods while the relative precision is best with prior sample degradation, approximately 5
percent, but less when the blood samples are run directly with the 1on exchange reagents
(Morrell and Giridhar, 1976), particularly at the low end of "noma!" blood lead values.
While AAS methods require attention to various spectral interferences to achieve satisfactory
performance, electrochemical methods such as ASV require consideration of such factors as the
effects of co-reducible metals and agents that complex lead and alter its reduction-oxidation
(redox) potential properties. Chelants used in therapy, particularly penicillamine, may In-
terfere, as does blood copper, which may be elevated in pregnancy and such disease states as
leukemia, lymphoma, and hyperthyroidism (Berman, 1981). At very low levels of lead in blood,
then, ASV may pose more problems than atomic absorption spectrometry techniques.
Correction of whole blood lead values for hematocrit, although carried out 1n the past,
is probably not appropriate and not commonly done at present. While the erythrocyte is the
carrier for virtually all lead, in blood, the saturation capacity of the red blood cell for
lead is so high that 1t can still carry lead even at highly toxic levels (Kochen and Greener,
1973). Kochen and Greener (1973) also showed that acute or chronic dosing at a given lead
level in rats with a wide range of hematocrits (Induced by bleeding) gave similar blood lead
values. Rosen et al. (1974), based on studies of hematocrit, plasma, and whole blood lead 1n
children, noted hematocrit correction was not necessary, a view supported by Chlsolm (1974).
9.2.2.2 Lead in Plasma. While virtually all of the lead present in whole blood Is bound to
the erythrocyte (Robinson et al., 1958; Kochen and Greener, 1973), lead In plasma 1s trans-
ported to affected tissues. It 1s very important, therefore, that every precaution be taken
23PB12/C 9-10 7/1/83
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PRELIMINARY DRAFT
to use non-hemolyzed blood samples for plasma isolation. The very low levels of lead in
plasma require that more attention be paid to "ultra clean" methods.
Rosen et al. (1974) used flameless atomic absorption spectrometry and microliter samples
of plasma to measure plasma lead, with background correction for the smoke signal generated
for the unmodified sample. Cavalleri et al. (1978) used a combination of solvent extraction
of modified plasma with preconcentrating and flameless atonic absorption. These authors noted
that the method used by Rosen et al. (1974) permitted less precision and accuracy than did
their technique, because a significantly smaller amount of lead was delivered to the furnace
accessory.
DeSilva (1981) used a technique similar to that of Cavalleri et al. (1978), but collected
samples in heparinized tubes, claiming that the use of EDTA as anticoagulant disturbs the
cell-plasma distribution of lead enough to yield erroneous data. Much more care was given in
this procedure to background contamination. In both cases, increasing levels of plasma lead
were measured with Increasing whole blood lead, suggesting an equilibrium ratio in contradic-
tion to the data of Rosen et al. (1974), who found a fixed level of 2-3 (jg Pb/dl plasma over a
wide range of blood lead. However, the actual levels of lead in plasma in the DeSilva (1981)
study were much lower than those reported by Cavalleri et al. (1978).
Using isotope-dilution mass spectrometry and sample collection/manipulation in an
"ultra-clean" facility, Everson and Patterson (1980) measured the plasma lead levels in two
subjects, a control and a lead-exposed worker. The control had a plasma lead level of 0.002
pg Pb/dl, several orders of magnitude lower than that seen with studies using less precise
analytical approaches. The lead-exposed worker had a plasma level of 0.2 pg Pb/dl. Several
other reports in the literature using isotope-dilution mass spectrometry noted somewhat higher
values of plasma lead (Manton and Cook, 1979; Rabinowitz et al., 1974), which Everson and
Patterson (1980) have ascribed to problems of laboratory contamination. Utilizing tracer lead
to minimize the impact of contamination results 1n a value of 0.15 pg/dl (Rabinowitz et al.,
1974).
With appropriate plasma lead methodology, reported lead levels are extremely low, the de-
gree varying with the methods used to measure such concentrations. While the data of Everson
and Patterson (1980) were obtained from only two subjects, it seems unlikely that using more
subjects would result in a plasma lead range extending upward to the levels seen with ordinary
methodology in ordinary laboratory surroundings. The above considerations are necessary when
discussing appropriate methodology for plasma analysis, and the Everson and Patterson (1980)
report indicates that some doubt surrounds results obtained with conventional methods. Al-
though not the primary focus of their study, the values obtained by Everson and Patterson
(1980) for whole blood lead, unlike the data for plasma, are within the ranges for unexposed
(11 pg Pb/dl) and exposed (80 pg Pb/dl) subjects generally reported with other methods. This
23PB12/C 9-11 7/1/83
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PRELIMINARY DRAFT
would suggest that, for the most part, reported values do actually reflect jn vivo blood lead
levels rather than sampling problems or inaccurate methods.
9.2.2.3 Lead in Teeth. When carrying out analysis of shed deciduous or extracted permanent
teeth, some reports have used the whole tooth after surface cleaning to remove contaminating
lead (e.g., Moore et al., 1978; Fosse and Justesen, 1978; Mackie et al., 1977), while others
have measured lead in dentine (e.g., Shapiro et al., 1973; Needleman et al., 1979; Al-Naimi et
al., 1980). Several reports (Grandjean et al., 197.8; Shapiro et al., 1973) have also de-
scribed the analysis of secondary (clrcumpulpal) dentine, that portion of the tooth found to
have the highest relative fraction of lead. Needleman et al. (1979) separated dentine by em-
bedding the tooth 1n wax, followed by thin central sagittal sectioning. The dentine was then
isolated from the sawed sections by careful chiseling.
The mineral and organic composition of teeth and their components requires the use of
thorough chemical decomposition techniques, including wet ashing and dry ashing steps, sample
pulverizing or grinding, etc. In the procedure of Steenhout and Pourtois (1981), teeth are
dry ashed at 4S0°C, powdered, and dry ashed again. The powder is then dissolved in nitric
acid. Fosse and Justesen (1978) reduced tooth samples to a coarse powder by crushing in a
vise, followed by acid dissolution. Oehme and Lund (1978) crushed samples to a fine powder in
an agate mortar and dissolved the samples 1n nitric acid. Mackie et al. (1977) and Moore et
al. (1978) dissolved samples directly in concentrated acids. ChatmSm and Wilson (1975) and
Needleman et al. (1974) carried out wet ashing with nitric acid followed by dry ashing at
450°C. Oehme and Lund (1978) found that acid wet ashing of tooth samples yielded better re-
sults 1f carried out 1n a heated Teflon bomb at 200°C.
With regard to methods of measuring lead In teeth, atomic absorption spectrometry and
anodic stripping voltamnetry have been employed most often. With the AAS methods, the high
mineral content of teeth tends to argue for Isolating lead from this matrix before analysis.
In Needleman et al.'s (1974) and Chatman and Wilson's (1975) method, ashed residues in nitric
acid were treated with ammonium nitrate and ammonium hydroxide to a pH of 2.8, followed by
dilution and extraction with a methylisobutylketone solution of ammonium pyrrolIdine-
carbodithioate. Analysis 1s by flame AAS using the 217.0 nm lead absorption line. A similar
procedure was employed by Fosse and Justesen (1978).
Anodic stripping voltammetry has been successfully used in tooth lead measurement
(Shapiro et al., 1973; Needleman et al., 1979; Oehme and Lund, 1978). As typified by the
method of Shapiro et al. (1973), samples of dentine were dissolved In a small volume of low-
lead concentrated perchloric acid and diluted (5.0 ml) with lead-free sodium acetate solution.
With deo*ygenat1on, samples were analyzed 1n a commercial ASV unit, using a plating time of 10
minutes at a plating potential of -1.05 V. Anodic sweeping was at a rate of 60 mV/sec with a
variable current of 100-500 pA.
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Since lead content of teeth is higher than in most samples of biological media, the rela-
tive precision of analysis with appropriate accommodation of the matrix effect, such as the
use of matrix-matched standards, in the better studies indicates a value of approximately 5-7
percent.
All of the above methods involve shed or extracted teeth and consequently provide a ret-
rospective determination of lead exposure. In Bloch et al.'s (1976) procedure, tooth lead is
measured j_n situ using an X-ray fluorescence technique. A col 1imated beam of radiation from
S7Co was allowed to irradiate the upper central incisor teeth of the subject. Using a rela-
tively safe 100-second irradiation time and measurement of and Ka2 lead lines via a ger-
manium diode and a pulse height analyzer for signal processing, lead levels of 15 ppm or
higher could be measured. Multiple measurement by this method would be very useful in pros-
pective studies because it would show the "on-going" rate of increase in body lead burden.
Furthermore, when combined with serial blood sampling, it would provide data for blood lead-
tooth lead relationships.
9.2.2.4 Lead in Hair. Hair constitutes a non-invasive sampling source with virtually no
problems with sample stability on extended storage. However, the advantages of accessibility
and stability are offset by the problem of assessing external contamination of the hair sur-
face by atmospheric fallout, hand dirt, lead in hair preparations, etc. Thus, such samples
are probably of less value overall than those from other media.
The various methods that have been employed for removal of external lead have been
reviewed (Chatt et al. , 1980; Gibson, 1980; Chattopadhyay et al., 1977). Cleaning techniques
obviously should be vigorous enough to remove surface lead but not so vigorous as to remove
the endogenous fraction. To date, it remains to be demonstrated that any published cleaning
procedure is reliable enough to permit acceptance of reported levels of lead in hair. Such a
demonstration would have to use lead isotopic studies with both surface and endogenous
isotopic lead removal monitored as a function of a particular cleaning technique.
9.2.2.5 Lead in Urine. Analysis of lead in urine is complicated by its relatively low con-
centrations (lower than in blood in many cases) as well as by the complex mixture of mineral
elements present. Lead levels are higher, of course, in cases where lead mobilization or
therapy with chelants is in progress, but in these cases samples must be analyzed to account
for lead bound to chelants such as EDTA. This requires either sample ashing or the use of
standards containing the chelant. Although analytical methods have been published for the
direct analysis of lead in urine, samples are probably best wet ashed before analysis, using
the usual mixtures of nitric plus sulfuric and/or perchloric acids.
Both atomic absorption spectrometric and anodic stripping voltammetric methods have been
applied to urine lead analyses, the former employing either direct analysis of ashed residues
or a preliminary chelation-extraction step. With flame AAS, ashed urine samples must invari-
23PB12/C 9-13 7/1/83
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PRELIMINARY DRAFT
ably be extracted with a chelant such as ammonium pyrrolidinecarbodithioate in methylisobutyl-
ketone to achieve reasonably satisfactory results. Direct analysis, furthermore, creates me-
chanical problems with burner operation, due to the high mineral content of urine, and results
in considerable maintenance problems with equipment. The procedure of Lauwerys et al. (1975)
is typical of flame AAS methods with preliminary lead separation. Owing to the relatively
greater sensitivity of graphite furnace (flameless) AAS, this variation of the method has been
applied to urine analysis in scattered reports where it appears that adequate performance for
direct sample analysis requires steps to minimize matrix interference. A typical example of
one of the better direct analysis methods is that of Hodges and Skelding (1981). Urine
samples were mixed with iodine solution and heated, then diluted with a special reagent con-
taining ammonium molybdate, phosphoric acid, and ascorbic acid. Small aliquots (5 pi) were
delivered to the furnace accessory of an AAS unit containing a graphite tube pretreated with
amnionium molybdate. The relative standard deviation of the method is reported to be about 6
percent. In the method of Legotte et al. (1980), such tube treatment and sample modifications
were not employed and the average precision figure was 13 percent.
Compared with various atomic absorption spectrometric methods, anodic stripping voltam-
metry has been less frequently employed for urine lead analysis, and it would appear from
available electrochemical methods in general that such techniques applied to urine require
further development. Franke and de Zeeuw (1977) used differential pulse anodic stripping vol-
tammetry as a screening tool for lead and other elements in urine. Jagner et al. (1979) de-
scribed analysis of urine lead using potentiometric stripping. In their procedure the element
was pre-concentrated at a thin-film mercury electrode as in conventional ASV, but deoxygenated
samples were reoxidized with either oxygen or mercuric ions after the circuitry was disconnec-
ted.
As noted in Section 9.1.1.2, spot sampling of lead in urine should be expressed per unit
creatinine, if it is not possible to obtain 24-hour collection.
9.2.2.6 Lead in Other Tissues. Bone samples of experimental animal or human autopsy origin
require preliminary cleaning procedures for removal of muscle and connective tissue, with care
being taken to minimize sample contamination. As is the case with teeth, samples must be che-
mically decomposed before analysis. Satisfactory instrumental methods for bone lead analysis
comprise a much smaller literature than is the case for other media.
Wittmers et al. (1981) have described the measurement of lead in dry-ashed (450°C) bone
samples using flameless atomic absorption spectrometry. Ashed samples were weighed and dis-
solved in dilute nitric acid containing lanthanum ion, the latter being used to suppress in-
terference from bone elements. Small volumes (20 pi) and high calcium content required that
atomization be done at 2400°C to avoid condensation of calcium within the furnace. Quantifi-
cation was by the method of additions. Relative precision was 6-8 percent at relatively high
lead content (60 pg/g astl) and 10-12 percent at levels of 14 yg/g ash or less.
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Ahlgren et al. (1980) described the application of X-ray fluorescence analysis to In vivo
lead measurement in the human skeleton, using tibia and phalanges. In this technique, ir-
radiation is carried out with dual B7Co gamma ray source. The generated KqV and Kffl2 lead
lines are detected with a lithium-drifted germanium.detector. The detection limit is 20 parts
per million.
Soft organs differ from other biological media in the extent of anatomic heterogeneity as
well as lead distribution, e.g., brain vs. kidney. Hence, sample analysis involves either
discrete regional sampling or the homogenizing of an organ. The efficiency of the latter can
vary considerably, depending on the density of the homogenate, the efficiency of rupture of
the formed elements, and other factors. Glass-on-glass homogenizing 1s to be avoided because
lead is liberated from the glass matrix with abrasion.
Atomic absorption spectrometry, in its flame or flameless variations, appears to be the
method of choice in many studies. In the procedure of Slavin et al. (1975), tissues were wet
ashed and the residues taken up in dilute acid and analyzed with the furnace accessory of an
AAS unit. A large number of reports representing slight variations of this basic technique
have appeared over the years (Lawrence, 1982, 1983). Flame procedures, being less sensitive
than the graphite furnace method, require more sample than may be available or are restricted
to measurement in tissues where levels are relatively high, e.g., kidney. In the method of
Farris et al. (1978), samples of brain, liver, lung, or spleen (as discrete segments) were
lyophilized and solubilized at room temperature with nitric acid. Following neutralization,
lead was extracted into methylisobutylketone with ammonium pyrrolidinecarbodithioate and
aspirated into the flame of an AAS unit. The reported relative precision was 8 percent.
9.2.3 Quality Assurance Procedures In Lead Analysis
Regardless of technical differences among the different methodologies for lead analysis,
one can define the quality of such techniques as being of: (1) poor accuracy and poor pre-
cision; (2) poor accuracy and good precision; or (3) good accuracy and good precision. In
terms of available information, the major focus in assessing quality has been on blood lead
determinations.
According to Boutwell (1976), the use of quality control testing for lead measurement
rests on four assumptions: (1) the validity of the specific procedure for lead in some matrix
has been established; (2) the stability of the factors making up the method has been both es-
tablished and manageable; (3) the validity of the calibration process and the calibrators with
respect to the media being analyzed has been established; and (4) surrogate quality control
materials of reliably determined analyte content can be provided. These assumptions, when
translated into practice, revolve around steps employed within the laboratory, using a battery
of "internal checks" and a further reliance on "external checks" such as a formal, well-
organized, multi-laboratory proficiency testing program.
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Analytical quality protocols can be further divided into start-up and routine procedures,
the former entailing the establishment of detection limits, "within-run" and "between-run"
precision, recovery of analyte, etc. When a new method is adopted for some specific analyti-
cal advantage, the procedure is usually tested in the laboratory or outside the laboratory for
comparative performance. For example, Hicks et al. (1973) and Kubasi k. et al. (1972) reported
that f1ameless techniques for measuring lead in whole blood were found to have a satisfactory
correlation with results using conventional flame procedures. Matson et al. (1970) noted a
good agreement between anodic stripping voltammetry and both atomic absorption spectral and
dithizone colorimetric techniques. The problem with such comparisons is that the reference
method is assumed to be accurate for the particular level of lead in a given matrix. High
correlations obtained in this manner may simply indicate that two inaccurate methods are
simultaneously performing with the same level of precision.
Preferable approaches for assessing accuracy are the use of certified samples determined
by a definitive method, or a direct comparison of different techniques with a definitive pro-
cedure. For example, Eller and Hartz (1977) compared the precision and accuracy of five
available methods for measuring lead in blood: dithizone spectrometry, extraction and tanta-
lum boat AAS, extraction and flame aspiration AAS, direct aspiration AAS, and graphite furnace
AAS techniques. Porcine whole blood certified by the National Bureau of Standards (NBS) using
isotope-dilution mass spectrometry at 1.00 yg Pb/g (±0.023) was tested and all methods were
found to be equally accurate. The tantalum boat technique was found to be the least precise.
The obvious limitation of these data is that they relate to a high blood lead content, suit-
able for use in measuring the exposure of lead workers or in some other occupational context,
but less appropriate for clinical or epidemiological investigations.
Boone et al. (1979) compared the analytical performance of 113 laboratories using various
methods and 12 whole blood samples (blood from cows fed a lead salt) certified as to lead con-
tent using isotope-dilution mass spectrometry at the NBS. Lead content ranged from 13 to 102
tjg Pb/dl, determined by anodic stripping voltammetry and five variations of AAS. The order of
agreement with NBS values, i.e., relative accuracy, was: extraction > ASV > tantalum strip >
graphite furnace > Oelves cup > carbon rod. The AAS methods all tended to show bias, being
positive at values less than 40 mq Pb/dl and negative at levels greater than 50 m9 Pb/dl. ASV
tended to show less of a positive bias problem, although it was not bias-free within either of
the blood lead ranges. In terms of relative precision, the ranking was: ASV > Delves cup >
tantalum strip > graphite furnace > extraction > carbon rod. The overall ranking in accuracy
and precision indicated: ASV > Delves cup > extraction > tantalum strip > graphite furnace >
carbon rod. As the authors cautioned, the above data should not be taken to indicate that any
established laboratory using one particular technique would not perform better than this;
rather, it should be used as a guide for newer facilities choosing among methods.
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There are a number of necessary steps In quality assurance pertinent to the routine
Measurement of lead that should be used In an ongoing program. With respect to Internal
checks of routine performance, these include calibration and precision and accuracy testing.
With biological matrices, the use of matrix-matched standards is quite important, as is an
understanding of the range of linearity and variation of calibration curve slopes frop day to
day. It is common practice to analyze a given sample in duplicate, further replication being
carried out if the first two determinations vary beyond a predetermined range. A second de-
sirable step is the analysis of samples collected in duplicate but analyzed "blind" to avoid
bias.
Monitoring of accuracy within the laboratory is limited to the availability of control
samples having a certified lead content in the sane medium as the samples being analyzed.
Controls should be as physically close to the media being analyzed as possible. Standard re-
ference materials (SRMs), such as orchard leaves and lyophilized bovine liver, are of help in
some cases, but there is need for NBS-certified blood samples for the general laboratory com-
munity. There are commercially available whole blood samples, prepared and certified by the
marketing facility (TOX-EL, A.R. Smith Co., Los Angeles, CA; Kaulson Laboratories, Caldwell,
NJ; Behringwerke AG, Marburg, W. Germany; and Health Research Institute, Albany, NY). With
these samples, attention must be paid to the reliability of the methods used by reference
laboratories. The use of such materials, from whatever source, must minimize bias; for exam-
ple, the attention given control specimens should be the same as that given routine samples.
Finally, the most important form of quality assurance is the ongoing assessment of lab-
oratory performance by proficiency testing programs using externally provided specimens for
analysis. Earlier interlaboratory surveys of lead measurement 1n blood and in urine indicated
that a number of laboratories had performed unsatisfactorily, even at high levels of lead
(Keppler et al., 1970; Donovan et al., 1971; Berlin et al., 1973), although there may have
been problems in the preparation and status of the blood samples during and after distribution
(World Health Organization, 1977). These earlier tests for proficiency indicated that: (1)
many laboratories were able to achieve a good degree of precision within their own facilities;
(2) the greater the number of samples routinely analyzed by a facility, the better the per-
formance; and (3) 30 percent of the laboratories routinely analyzing blood lead reported
values differing by more than 15 percent from the true level (Pierce et al., 1976).
In the more recent, but very limited, study of Paulev et al. (1978), five facilities par-
ticipated in a survey, using samples to .which known amounts of lead were added. For lead in
both whole blood and urine, the interlaboratory coefficient of variation was reported to be
satisfactory, ranging from 12.3 to 17.2 percent for blood and urine samples. Aside from Its
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limitation of scope, this study used "spiked" Instead of jm vivo lead, so that extraction
techniques used in most of the laboratories surveyed would have given misleadingly better
results in terms of actual recovery.
Maher et al. (1979) described the outcome of a proficiency study involving up to 38 lab-
oratories that analyzed whole blood pooled from a large number of samples submitted for blood
lead testing. The Delves cup technique was the most heavily represented, followed by the
chelatlon-extraction plus flame AAS method and the graphite furnace AAS method. Anodic strip-
ping voltammetry was used by only approximately 10 percent of the laboratories, so that the
results basically portray AAS methods. All laboratories had about the same degree of ac-
curacy, with no evidence of consistent bias, while the interlaboratory coefficient of
variation was approximately 15 percent. A subset of this group, certified by the American
Industrial Hygiene Association (AIHA) for air lead, showed a corresponding precision figure of
approximately 7 percent. Over time, the subset of AIHA-certified laboratories remained about
the same 1n proficiency, while the other facilities showed continued Improvement in both ac-
curacy and precision. This study indicates that program participation does help the per-
formance of a laboratory doing blood lead determinations.
The most comprehensive proficiency testing program is that carried out by the Centers for
Disease Control of the U.S. Public Health Service. This consists of two operationally and ad-
ministratively distinct subprograms, one conducted by the Center for Environmental Health
(CEH) and the other by the Licensure and Proficiency Testing Division, Laboratory Improvement
Program Office (LIPO). The CEH program is directed at facilities Involved in lead poisoning
prevention and screening, while LIPO is concerned with laboratories seeking certification
under the Clinical Laboratories Improvement Act of 1967 as well as under regulations of the
Occupational Safety and Health Administration (QSHA). Both the CEH and LIPO protocols involve
the use of bovine whole blood certified as to content by reference laboratories (6 in the CEH
program, 20-23 in LIPO) with an ad hoc target range of ±6 pg Pb/dl for values of 40 MS Pb/dl
or less and ±15 percent for higher levels. Three samples are provided monthly from CEH, for
a total of 36 yearly, while LIPO participants receive 3 samples quarterly (12 samples yearly).
Use of a fixed range rather than a standard deviation has the advantage of allowing the moni-
toring of overall laboratory improvement.
For Fiscal Year (FY) 1981, 114 facilities were in the CEH program, 92 of them partici-
pating for the entire year. Of these, 57 percent each month reported all three samples within
the target range, and 85 percent on average reported two out of three samples correctly. Of
the facilities reporting throughout the year, 95 percent had a 50 percent or better perfor-
mance, i.e., 18 blood samples or better. If one compares these summary data for FY 1981 with
earlier annual reports, it would appear that there has been considerable improvement in the
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PRELIMINARY DRAFT
number of laboratories achieving higher levels of proficiency. For the Interval FY 1977-79,
there was a 20 percent Increase In the number correctly analyzing more than 80 percent of all
samples and a 33 percent decrease 1n those reporting less than 50 percent correct. In the
last several years, FY 1979-81, overall performance appears to. have more or less stabilized.
With the LIPO program for 1981 (Dudley, 1982), the overall laboratory performance
averaged across all quarters was 65 percent of the laboratories analyzing all samples cor-
rectly and approximately 80 percent performing well with two of three samples. Over the four
years of this program, an Increasing ability to correctly analyze lead in blood appears to
have been demonstrated. Dudley's survey (1982) also indicates that reference laboratories in
the LIPO program are becoming more accurate relative to isotope-dilution mass spectrometry
values, I.e., bias over the blood lead range 1s contracting.
Current OSHA criteria for certification of laboratories measuring occupational blood lead
levels require that eight of nine samples be correctly analyzed 1n the previous quarter (U.S.
Occupational Safety and Health Administration, 1982). These criteria appear to reflect the
ability of a number of laboratories to perform at this level.
It should be noted that most proficiency programs, Including the CEH and LIPO surveys,
are appropriately concerned with blood lead levels encountered in such cases as pediatric
screening for excessive exposure to lead or in occupational exposures. As a consequence,
there does appear to be an underrepresentatlon of lead values 1n the low end of the "normal"
range. In the CEH distribution for FY 1981, four samples (11 percent) were below 25 pg Pb/dl.
The relative performance of the 114 facilities with these samples indicates outcomes much
better than with the whole sample range.
9.3 DETERMINATION OF ERYTHROCYTE PORPHYRIN (FREE ERYTHROCYTE PROTOPORPHYRIN,
ZINC PROTOPORPHYRIN)
9.3.1 Methods of Erythrocyte Porphyrin Analysis
Lead exposure results In inhibition of the final step In heme biosynthesis, the insertion
of iron into protoporphyrin IX to form heme. This leads to an accumulation of the porphyrin,
with zinc (II) occupying the position normally filled by iron. Depending on the particular
method of analysis, zinc protoporphyrin (2PP) itself or the metal-free form, free erythrocyte
protoporphyrin (FEP), is measured. FEP generated as a consequence of chemical manipulation
should be kept distinct from the metal-free form biochemically produced in the porphyria,
erythropoietic protoporphyria. The chemical or "wet" methods measure free erythrocyte
porphyrin or zinc protoporphyrin, depending upon the relative acidity of the extraction
medium. The hematofluorometer in its commercially available form measures zinc proto-
porphyrin.
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PRELIMINARY DRAFT
Porphyrins are labile due to photochemical decomposition; hence, samples must be pro-
tected from light during collection and handling and analyzed as soon as possible.
Hematocrits must also be obtained to adjust for anemic subjects.
In terms of methodological approaches for EP analysis, virtually all methods now in use
exploit the ability of porphyrins to undergo intense fluorescence when excited at the appro-
priate wavelength of light. Such fluorometric techniques can be further classified as wet
chemical micromethods or as micro methods using a recently developed instrument, the hemato-
fluorometer. The latter involves direct measurement 1n whole blood. Because the mammalian
erythrocyte contains all of the EP in whole blood, either packed cells or whole blood may be
used, although the latter is more expedient.
Oue to the relatively high sensitivity of fluorometric measurement for FEP or ZPP,
laboratory methods for spectrof1uorometric analysis require a relatively small sample of
blood; hence, microtechniques are currently the most popular In most laboratories. These In-
volve either liquid samples or blood collected on filter paper, the latter of use particularly
in field sampling.
As noted above, chemical methods for EP analysis measure either free erythrocyte proto-
porphyrin, where zinc is chemically removed, or zinc protoporphyrin, where zinc is retained.
The procedures of Piomelli and Davidow (1972), Granick et al., (1972), and Chisholm and Brown
(1975) typify "free" EP methods, while those of Lamola et al. (1975), Joselow and Flores
(1977), and Chisholm and Brown (1979) involve measurement of zinc-EP.
In Piomelli and Davidow's (1972) micro procedure, small volumes of whole blood, analyzed
either directly or after collection on fiIter paper, were treated with a suspension of Celite
in saline followed by a 4:1 mixture of ethyl acetate to glacial acetic acid. After agitation
and centrlfugation, the supernatant was extracted with 1.5N HC1. The acid layer was analyzed
fluorometrically using an excitation wavelength of 405 nm and measurement at 615 nm. Blood
collected on filter paper discs was first eluted with 0.2 ml H20. The filter paper method was
found to work just as well as liquid samples of whole blood. Protoporphyrin IX was employed
as a quantitative standard. Granick et al. (1972) use similar microprocedure, but it differs
in the concentration of acid employed and the use of a ratio of maxima.
In Chisolm and Brown's (1975) variation, volumes of 20 pi of whole blood were treated
with ethyl acetate/acetic add (3:1) and briefly mixed. The acid extraction step was done
with 3N HC1, followed by a further dilution step with more acid if the value was beyond the
range of the calibration curve. In this procedure, protoporphyrin IX was used as the working
standard, with coproporphyrln used to monitor the calibration of the fluorometer and any
variance with the protoporphyrin standard.
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The above microfluorometric methods all involve double extraction. In the single-
extraction variation of Orfanos et al. (1977), liquid samples of whole blood (40 h1) or blood
on filter paper were treated with acidified ethanol, the mixtures agitated and centrlfuged,
and the supernatants analyzed directly in fluorometer cuvettes. For blood samples on filter
paper, blood was first leached from the paper with saline by soaking for 60 minutes. Copro-
porphyria was used as the quantitative standard. The correlation coefficient with the
PiomeTIi and Davidow (1972) procedure (see above) over the range 40-650 h9 EP/dl RBCs was
r = 0.98.
Lamola et al. (1975) analyzed the zinc protophyrin as such in their procedure. Small
volumes of blood (20 pi) were worked up in a detergent (dimethyl dodecylamine oxide) and
phosphate buffer solution, and fluorescence measured at 594 ran with excitation at 424 nm. In
the variation of Joselow and Flores (1977), 10 pi of whole blood was diluted 1000-fold, along
with protoporphyrin (Zn) standards, with the detergent-buffer solution. It should be noted
that it is virtually impossible to obtain the ZPP standard in pure form, and Chisolm and Brown
(1979) reported the use of protoporphyrin IX plus very pure zinc salt for such standards.
Regardless of the extraction methods used, some instrumental parameters are of impor-
tance, including the variation between cut-offs in secondary emission filters and variation
among photomultiplier tubes in the red region of the spectrum. Hanna et al. (1976) compared
four mlcromethods for EP analysis: double extraction with ethyl acetate/acetic acid and HC1
(Piomelli and Davidow, 1972), single extraction with either ethanol or acetone (Chisolm et
al., 1974), and direct solubilization with detergent (Lamola et al., 1975). Of these, the
ethyl acetate and ethanol procedures were satisfactory; complete extraction occurred only with
the ethylacetate/acetic add method. In the method of Chisholm et al. (1974), it appears that
the choice of acid and its concentration is more significant than the choice of organic
solvent.
The levels of precision with these wet mlcromethods appears to differ with the specifics
of analysis. Piomelll (1973) reported a coefficient of variation (C.V.) of 5 percent, com-
pared to Herber*s (1980) observation of 2-4 percent for the methods per se and 6-11 percent
total C.V., which included precision of samples, standards, and day-to-day variation. The
Lamola et al. (1975) method for ZPP measurement was found to have a C.V. of 10 percent (same
day, presumably), whereas Herber (1980) reported a day-to-day C.V. of 9.3-44.6 percent.
Herber (1980) also found that the wet chemical micro method of Piomelll (1973) had a detection
limit of 20 m9 EP/dl whole blood, while that of Lamola et al. (1975) was sensitive to 50 pg
EP/dl whole blood.
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PRELIMINARY DRAFT
The recent development of direct instrumental measurement of ZPP with the hematofluoro-
meter has added a dimension to the use of EP measurement for field screening the lead exposure
of large groups of subjects. As originally developed by Bell Laboratories (Blumberg et al.,
1977) and now produced commercially, the apparatus employs front-face optics, in which exci-
tation of the fluorophore is at an acute angle to the sample surface, with emitted light
emerging from the same surface and thus being detected. Routine calibration requires a stable
fluorescing material with spectra comparable to ZPP; the triphenyl methane dye Rhodanine B is
used for this purpose. Absolute calibration requires adjusting the microprocessor-controlled
readout system to read the known concentration of ZPP in reference blood samples, the latter
calibration being performed as frequently as possible.
Hematof1uorometers are designed for the measurement of EP in samples containing oxyhemo-
globin, I.e., capillary blood. Venous blood, therefore, must first be oxygenated, usually by
moderate shaking for approximately 10 minutes (Blumberg et al., 1977; Grandjean and Lintrup,
1978). A second problem with hematofluorometer use, in contrast to wet chemical methods, is
interference by bilirubin (Karacfc et al., 1980; Grandjean and Lintrup, 1978); this would oc-
cur with relatively low levels of EP. At levels normally encountered 1n lead workers or sub-
jects with anemia or nonoccupational lead exposure, the degree of such Interference 1s not
considered significant (Grandjean and Lintrup, 1978). Karacic et al. (1980) have found that
carboxyhemoglobln (COHb) may pose a potential problem, but its relevance to EP levels of sub-
jects exposed to lead has not been fully elucidated. Background fluorescence in cover glass
may be a problem and should be tested in advance. Finally, the accuracy of the heiatofluoro-
meter appears to be affected by hemolyzed blood.
Competently employed, the hematofluorometer appears to be reasonably precise but its ac-
curacy may still be biased (see below). Blumberg et al. (1977) reported a C.V. of 3 percent
over the entire range of ZPP values measured when using a prototype apparatus. Karacic et al.
(1980) found the relative standard deviation to vary from 1 percent (0.92 mM ZPP/M Hb) to 5
percent (0.41 mM ZPP/M Hb) depending on concentration. Grandjean and Lintrup (1978) obtained
a day-to-day C.V. of 5 percent using blood samples refrigerated for up to 9 weeks. Herber
(1980) obtained a total C.V. of 4.1-11.5 percent.
A number of investigators ¦ have compared EP measured by the hematof luorometer with the
laboratory or wet chemical techniques, ranging from a single, intralaboratory comparison to
interlaboratory performance testing. The latter included the EP proficiency testing program
of the Centers for Disease Control. Working with prototype instrumentation, Blumberg et al.
(1977) obtained correlation coefficients of r = 0.98 (range: 50-800 pg EP/dl RBCs) and 0.99
(range: up to 1000 pg EP/dl RBCs) for comparisons with the Granlck and Piomelli methods,
respectively. Grandjean and Lintrup (1978), Castoldi et al. (1979) and Karacid et al. (1980)
have achieved equally good correlation results.
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PRELIMINARY DRAFT
Several reports (Culbreth et al., 1979; Scoble et al., 1981; Smith et al., 1980) have
described the application of high-performance liquid chromatography (HPLC) to the analysis of
either free or zinc protoporphyrin 1n whole blood. In one of the studies (Scoble et al.,
1981), the protoporphyrins as well as coproporphyrin and mesoporphyrln IX were reported to be
determined on-line f1uorometrically In less than 6 minutes using 0.1 ml of blood sample. The
HPLC approach renalns to be tested in 1nterlaboratory proficiency programs.
9.3.2 Interlaboratory Testing of Accuracy and Precision in EP Measurement
In a relatively early attempt to assess 1nterlaboratory proficiency in EP measurement,
Jackson (1978) reported results of a survey of 65 facilities that analyzed 10 whole blood
samples by direct measurement with the heraatof 1 uorometer or by one of the wet chemical
methods. In this survey, the instrumental methods had a low bias compared to the extraction
techniques but tended to show better 1nterlaboratory correlation.
At present, CDC1s ongoing EP proficiency testing program constitutes the most comprehen-
sive assessment of laboratory performance (U.S. Centers for Disease Control, 1981). Every
month, three samples of whole blood prepared at the University of Wisconsin Laboratory of
Hygiene are forwarded to participants. Reference means are determined by a group of reference
laboratories with a target range of ±15 percent across the whole range of EP values. For
Fiscal Year 1981, of the 198 laboratories participating, 139 facilities were involved for the
entire year. Three of the 36 samples in the year were not included. Of the 139 year-long
participants, 93.5 percent had better than half of the samples within the target range, 84,2
percent performed satisfactorily with 70 percent or more of the samples within range, and 50.4
percent of all laboratories had 90 percent or more of the samples yielding the correct re-
sults. The participants as a whole showed greater proficiency than in the previous year. Of
the various methods currently used, the hematof1uorometer direct measurement technique was
most heavily represented. For example, the January 1982 survey of the three major techniques
154 participants used the hematof 1 uorometer, 30 used the PiomelH method, and 7 used the
Chisolm/Brown method.
The recent survey of Balamut et al. (1982) raises the troublesome observation that the
use of commercially available hematofluorometers may yield satisfactory proficiency results
but still be inaccurate when compared to the wet chemical method using freshly-drawn whole
blood. Two hematof1uorometers in wide use performed well in proficiency testing but showed an
approximately 30 percent negative bias with clinical samples analyzed by both instrument and
chemical microtechniques. This bias leads to false negatives when used In screening. It ap-
pears that periodic testing of split samples by both fluorometer and chemical means is neces-
sary to monitor, and correct for, instrument negative bias. The basis of the bias is much
more than can be explained by the difference between FEP and ZZP.
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9.4 MEASUREMENT OF URINARY COPROPORPHYRIN
The elevation of urinary coproporphyrln (CP-U) with lead Intoxication served as a useful
Indicator of such Intoxication in children and lead workers for many years. Although analysis
of CP-U has declined considerably in recent times with the development of other testing
methods, such as measurement of erythrocyte protoporphyrin, it still possesses the advantage
of showing active intoxication (Piomelli and Grazlano, 1980).
The standard method of CP-U determination 1s the fluorometric procedure described by
Schwartz et al. (1951). Urine samples are treated with acetate buffer and aqueous iodine, the
latter converting coproporphyrlnogen to CP. The porphyrin 1s partitioned Into ethyl acetate
and back-extracted (4 X) with 1.5N HC1. Coproporphyrln 1s employed as the quantitative stan-
dard. Working curves are linear below 5 pg CP/1 urine.
In the absorption spectrometric technique of Haeger-Aronsen (1960), Iodine 1s also used
to convert coproporphyrlnogen to CP. The extractant 1s ethyl ether, from which the CP is re-
moved with 0.IN HC1. Absorption is read at three wavelengths, 380, 430, and the Soret maximum
at 402 ran; and quantification is carried out using an equation involving the three wave
lengths.
9.5 MEASUREMENT OF DELTA-AMINOLEVULINIC ACID DEHYDRASE ACTIVITY
Delta-aminolevulinic acid dehydrase (5-aminolevulinate hydrolase; porphobilinogen
synthetase; E.C. 4.2.1.24; ALA-D) Is an allosterlc sulfhydryl enzyme that mediates the con-
version of two units of 6-am1nolevul1n1c acid to porphobilinogen, a precursor 1n the heme bio-
synthetic pathway to the porphyrins. Lead's inhibition of the activity of this enzyme 1s the
enzymological basis of ALA-D's diagnostic utility 1n assessing lead exposure using erythro-
cytes.
A number of sampling precautions are necessary when measuring this enzyme's activity.
ALA-D activity is modified by the presence of zinc as well as by lead. Consequently, blood
collection tubes that have high background zinc content, mainly in the rubber stoppers, must
be avoided completely or care taken to avoid stopper contact with blood. Nackowskl et al.
(1977) observed that the presence of zinc in blood collection tubes is a pervasive problem,
and 1t appears that plastic-cup tubes are the only practical means to avoid it. To guard
against zinc in the tube Itself, it would appear prudent to determine the extent of zinc
leachabllity by blood and to use one tube lot, if possible. Heparin Is the anticoagulant of
choice, as the lead binding agent, EDTA, or other chelants would affect the lead-enzyme inter-
action. The relative stability of the enzyne 1n blood makes rapid determinations of activity
necessary, preferably as soon after collection as possible. Even with refrigeration, analysis
of activity should be done within 24 hours (Berlin and Schaller, 1974). Furthermore, porpho-
bilinogen is light-labile, which requires that the assay be done under restricted light.
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PRELIMINARY DRAFT
Various procedures for ALA-0 activity measurement are chemically based on measurement of
porphobilinogen generated from the substrate, 6-ALA porphobilinogen is condensed with p-di-
methylaminobenzaldehyde (Ehrllch's reagent) to yield a chromophore measured at 553 n« in a
spectrophotometer. In the European Standardized Method for ALA-D activity measurement (Berlin
and Schaller, 1974), developed with the collaboration of nine laboratories for use with blood
samples having relatively low lead content, triplicate blood samples (0.2 ml) are heroolyzed,
along with a blood blank, with water for 10 minutes at 37°C. Samples are then mixed with
6-ALA solution followed by a 60-minute incubation. The enzyme reaction is terminated by ad-
dition of a solution of mercury (II) in trichloroacetic acid, followed by centrifugation and
filtration. Filtrates are mixed with modified Ehrlich's reagent (p-dimethylaminobenzalehyde
in trichloroacetic/perchloric acid mixture) and allowed to react for 5 minutes, followed by
chromophore measurement in a spectrophotometer at 555 nm. Activity is quantified in terms of
pM 6-ALA/min-l erythrocytes. It should be noted that the amount of phosphate for Solution A
in Berlin & Schaller1 s report should be 1.78 g, not the 1.38 g stated. In a micro scale
variation, Granick et al. (1973) used only 5 pi of blood and terminated the assay by tri-
chloroacetic acid.
In comparing various reports concerning the relationship between lead exposure and ALA-D
Inhibition, attention should be paid to the units of activity measurement employed with the
different techniques. Berlin and Schaller's (1974) procedure expresses activity as pM
ALA/min/1 cells, while Tomokuni1s (1974) method expresses activity as pM porphobi1inogen/hr/ml
cells. Similarly, when comparing the Bonslgnore et al. (1965) procedure to that of Berlin and
Schaller (1374), a conversion factor of 3.8 is necessary when converting from Bonslgnore to
European Standard Method units (Trevisan et al., 1981).
Several factors have been shown to affect ALA-D activity. Rather than measuring enzyme
activity in blood once, Granick et al. (1973) measured activity before and after treatment
with dithiothreitol, an agent that reactivates the enzyme by complexlng lead. The ratio of
activated to unactivated enzymes vs. blood lead levels accommodates inherent differences in
enzyme activity among individuals due to genetic factors and other reasons. Other agents for
such activation include zinc (Flnelli et al., 1975) and zinc plus glutathione (Mitchell et
al,, 1977). In the Mitchell et al. (1977) study, non-physiological levels of zinc were used.
Wigfield and Farant (1979) found that enzyme activity is related to assay pH; thus, reduced
activity from such a pH-activity relationship could be misinterpreted as lead inhibition.
These researchers find that pH shifts away from optimal, in terms of activity, as blood lead
content increases and the incubation step proceeds.
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9.6 MEASUREMENT OF DELTA-AMINOLEVULINIC ACID IN URINE AND OTHER MEDIA
Delta-aminolevulinic acid (fi-ALA) levels Increase with elevated lead exposure, due to the
inhibitory effect of lead on the activity of ALA dehydirase and/or the Increase of ALA synthe-
tase activity by feedback derepression. The result 1s that this Intermediate 1n heme bio-
synthesis rises 1n the body and eventually results in Increased urinary excretion. The meas-
urement of this metabolite in urine provides an indication of the level of lead exposure.
The ALA content of urine samples 1s stable for approximately 2 weeks or more if urine
samples are acidified with tartaric or acetic acid and kept refrigerated. Values of ALA-U are
adjusted for urine density, if concentration 1s expressed In mg/1 or is measured per gram
creatinine. As noted in the case of urinary lead measurement, 24-hour collection 1s more de-
sirable than spot sampling.
Five manual and one automated procedure for urinary ALA measurement are most widely used.
Mauzerall and Granlck (1956) and Davis and Andelman (1967) described the most involved proce-
dures, requiring the Initial chromatographic separation of ALA. The approach of Grabeckl et
al. (1967) omitted chromatographic isolation, whereas the automated variation of Lauwerys et
al. (1972) omitted prechromatography but included the use of an Internal standard. Tomokuni
and Ogata (1972) omitted, chromatography but employed solvent extraction to isolate the pyr-
role Intermediate.
Mauzerall and Granlck (1956) condensed ALA with a p-dicarbor\yl compound, acetylacetone,
at pH 4.6 to yield a pyrrole Intermediate (Knorr condensation reaction), which was further re-
acted with p-d1methyl aminobenzaldehyde 1n perchloric/acetic acid. The samples were then read
in a spectrophotometer at 553 nm 15 minutes after mixing. In this method, there Is separation
of both porphobilinogen and ALA from urine by means of a dual column configuration of cation
and anion exchange resins. The latter retains the porphobilinogen and the former separates
ALA from urea. The detection limit is 3 pmoles/1 urine. In the modification of this method
by Davis and Andelman (1967), disposable cat1on/an1on resin cartridges were used, in a
sequential configuration, to expedite chromatographic separation and Increase sample analysis
rate. Commercial (Blo-Rad) disposable columns based on this design are now available and
appear satisfactory.
In these two approaches (Mauzerall and Granlck, 1956; Davis and Andelman^ 1967), the pro-
blem of Interference due to aminoacetone, a metabolite occurring 1n urine, is not taken into
account. However, Marver et al. (1966) used Dowex-1 in a chromatographic step subsequent to
the condensation reaction to form the pyrrole. This separates the ALA derivative from that of
the amlnoacetone. Similarly, Schlenker et al. (1964) used an IRC column to retain amino-
acetone.
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Tomokuni and Ogata (1972) condensed ALA with ethylacetoacetate and extracted the re-
sulting pyrrole with ethyl acetate. The extract was then treated with Ehrllch's reagent and
the resulting chromophore measured spectrophotometries!ly. Lauwerys et al. (1972) developed
an automated ALA analysis method for lead worker screening, in which ALA was added in known
amount as an internal standard and the pre-chromatography avoided. They reported a high cor-
relation (r = 0.98, no range available) with the procedure of Hauzerall and Granick (1956).
Roels et al. (1974) compared the relative proficiency of four methods — those of
Hauzerall and Granick (1956), Davis and Andelman (1967), the Lauwerys et al. (1972) automated
version, and the Grabecki et al. (1967) method, which omits chromatographic separation and is
normally used with occupational screening. The chromatographic methods gave identical results
over the range of 0-60 mg ALA/1 urine, while the automated method showed a positive bias at <6
mg/1. The Grabecki et al. (1967) technique was the least satisfactory of the procedures com-
pared. Roels et al. (1974) also noted that commercial ion-exchange columns resulted in low
variability (<10 percent).
Della-Fiorentina et al. (1979) combined the Tomokuni and Ogata (1972) extraction method
with a correction equation for urine density. Up to 25 ng ALA/1, the C.V. was S4 percent
along with a good correlation (r = 0.937) with the Davis and Andelman (1967) technique. While
there is a time saving in avoiding prechromatography, it is necessary to prepare a curve re-
lating urine density to a correction factor for quantitative measurement.
Although ALA analysis is nprmally done with urine as the indicator medium, Haeger-Aronsen
(1960) reported a similar colorlmetric method for blood and MacGee et al. (1977) described a
gas-liquid chromatographic method for ALA In plasma as well as urine. Levels of ALA in plasma
are much lower than those In urine. In the latter method, ALA was isolated from plasma, re-
acted with acetyl-acetone, and partitioned into a solvent (trimethylphenylhydroxlde), which
also served for pyrolytic methylation in the injection port of the gas-liquid chromatograph,
the methylated pyrrole being more amenable to chromatographic isolation than the more polar
precursor. #For quantification, an internal standard, 6-an1no-5-oxohexano1c acid, was used.
The sample requirement is 3 ml plasma. Measured levels ranged from 6.3 to 73.5 ng ALA/ml
plasma, and yielded values that were approximately 10-fold lower than the colorlmetric techni-
ques (0'Flaherty et al., 1980).
9.7 MEASUREMENT OF PYRIMIDINE-5'-NUCLEOTIDASE ACTIVITY
Erythrocyte pyr1midine-5'-nucleotidase (5'-ribonucleotide phosphohydrolase, E.C. 3.1.3.5,
Py5N) catalyzes the hydrolytic dephosphorylation of the pyrlmidlne nucleotides uridine mono-
phosphate (UMP) and cytidinemonophosphate (CMP) to uridine and cytldlne (Paglla and Valentine,
1975). Enzyme inhibition by lead in humans and animals results In Incomplete degradation of
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PRELIMINARY DRAFT
reticulocyte RNA fragments, accumulation of the nucleotides, and increased cell hemolysis
(Paglia et al., 1975; Paglia and Valentine, 1975; Angle and Mclntire, 1978; George and Duncan,
1982).
There are two methods for measurement of Py5N activity. One is quite laborious in terms
of time and manipulation, while the other is shorter but requires the use of radioisotopes and
radiometric measurement. In Paglia and Valentine's (1975) method, heparinlzed venous blood
was filtered through cotton or a commercial cellulose preparation to separate erythrocytes
from platelets and leukocytes. Cells were given multiple saline washings, packed lightly, and
subjected to freeze hemolysis. The hemolysates were dialyzed against a saline-Tris buffer
containing MgCl2 and EDTA to remove nucleotides and other phosphates. The assay system con-
sists of dialyzed hemolysate, MgCl2, Tris buffer at pH 8.0, and either UMP or CMP; incubation
is for 2 hours at 37°C. Activity is terminated by treatment with 20 percent trichloroacetic
acid, followed by centrifugation. The supernatant inorganic phosphate, P.., is measured by the
classic method of Fiske and Subbarow (1925), the phosphomolybdic acid complex being measured
spectrophotometrically at 660 nm. A unit of enzyme activity is expressed as pmol P^/hr/g
hemoglobin. Hemolysates appear to be stable (90 percent) with refrigeration at 4°C for up to
6 days, provided that mercaptoethanol is added at_ the time of assay. Like the other method,
activity measurement requires the determination of hemoglobin.
In the simpler approach of Torrance et al. (1977), which can be feasibly applied to much
larger numbers of samples, erythrocytes were separated from leukocytes and platelets with a
1:1 mixture of microcrystalline and alphacellulose, followed by saline washing and hemolysis
with a solution of mercaptoethanol and EDTA. Hemolysates were incubated with a medium con-
taining purified "C-CMP and MgCl2 for 30 minutes at 37°C. The reaction was terminated by
sequential addition of barium hydroxide and zinc sulfate solution. Proteins and unreacted
nucleotide were precipitated, leaving the labeled cytidine in the supernatant. Aliquots were
measured for ,4C activity in a liquid scintillation counter. Enzyme activity was expressed as
nM CMP/min/g hemoglobin. The blank activity was determined for each sample by carrying out
the precipitation step as soon as the hemolysate was mixed with the labeled CMP, i.e., t = 0.
This procedure shows a good correlation (r = 0.94; range: 135-189 enzyme units) with the
method of Paglia and Valentine (1975). The two methods express units of enzyme activity dif-
ferently, so that one must know which method is used when comparing enzyme activity.
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9.8 SUMMARY
The sine qua non of a complete understanding of a toxic agent's effects on an organisn,
e.g., dose-effect relationships, is quantitative Measurement of either that agent in some bio-
logical medium or a physiological parameter associated with exposure to the agent. Quantita-
tive analysis involves a number of discrete steps, all of which contribute to the overall
reliability of the final analytical result: sample collection and shipment, laboratory
handling, instrumental analysis, and criteria for internal and external quality control.
From a historical perspective, it is clear that the definition of "satisfactory analyt-
ical method" for lead has been steadily changing as new and more sophisticated equipment
becomes available and understanding of the hazards of pervasive contamination along the
analytical course increases. The best example of this is the use of the definitive method for
lead analysis, isotope-dilution mass spectrometry in tandem with "ultra-clean" facilities and
sampling methods, to demonstrate conclusively not only the true extent of anthropogenic input
of lead to the environment over the years but also the relative limitations of most of the
methods for lead measurement used today.
9,8.1 Determinations of lead in Biological Media
The low levels of lead in biological media, even in the face of excessive exposure, and
the fact that sampling of such media must be done against a backdrop of pervasive lead contam-
ination necessitates that samples be carefully collected and handled. Blood lead sampling is
best done by venous puncture and collection into low-lead tubes after careful cleaning of the
puncture site. The use of finger puncture as an alternative method of sampling should be
avoided, 1f feasible, given the risk of contamination associated with the practice in indus-
trialized areas. While collection of blood onto filter paper enjoyed some popularity in the
past, paper deposition of blood requires special correction for hematrocrit/hemoglobin level.
Urine sample collection requires the use of lead-free containers as well as addition of a
bactericide. If feasible, 24-hour sampling is preferred to spot collection. Deciduous teeth
vary in lead content both within and across type of dentition. Thus a specific tooth type
should be uniformly obtained for all study subjects and, if possible, more than a single
sample should be obtained from each subject.
Measurements of Lead in Blood. Many reports over the years have purported to offer
satisfactory analysis of lead in blood and other biological media, often with severe inherent
limitations on accuracy and precision, meager adherence to criteria for accuracy and pre-
cision, and a limited utility across a spectrum of analytical applications. Therefore, it is
only useful to discuss "definitive" and, comparatively speaking, "reference" methods presently
used.
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In the case of lead In biological media, the definitive method 1s 1sotope-d11ut1on mass
spectrometry (IDHS). The accuracy and unique precision of IDMS arise from the fact that all
manipulations are on a weight basis involving simple procedures, and measurements entail only
lead isotope ratios and not the absolute determinations of the Isotopes Involved, greatly re-
ducing Instrumental corrections and errors. Reproducible results to a precision of one part
In 104-105 are routine with appropriately designed and competently operated instrumentation.
Although this methodology is still not recognized in many laboratories, 1t was the first
breakthrough, in tandem with "ultra-clean" procedures and facilities, to definitive methods
for indexing the progressive increase in lead containlnation of the environment over the
centuries. Given the expense, required level of operator expertise, and time and effort
involved for measurements by IDMS, this methodology mainly serves for analyses that either
require extreme accuracy and precision, e.g., geochronometry, or for the establishment of
analytical reference material for general testing purposes or the validation of other
methodologies.
While the term "reference method" for lead in biological media cannot be rigorously ap-
plied to any procedures 1n popular use, the technique of atomic absorption spectrometry in Its
various configurations or the electrochemical method, anodic stripping voltammetry, come
closest to meriting the designation. Other methods that are generally applied in metal anal-
yses are either United in sensitivity or are not feasible for use on theoretical grounds for
lead analysis.
Atomic absorption spectrometry (AAS) as applied to analysis of whole blood generally in-
volves flame or flameless mlcromethods. One macromethod, the Hessel procedure, still enjoys
some popularity. Flame microanalysis, the Delves cup procedure, applied to blood lead appears
to have an operational sensitivity of about 10 pg Pb/dl blood and a relative precision of
approximately 5 percent 1n the range of blood lead seen in populations 1n industrialized
areas. The flameless, or electrothermal, method of AAS enhances sensitivity about 10-fold,
but precision can be more problematical because of chemical and spectral Interferences.
The most widely used and sensitive electrochemical method for lead in blood is anodic
stripping voltammetry (ASV). For most accurate results, chemical wet ashing of samples must
be carried out, although this .process 1s t1me-consuai1ng and requires the use of lead-free
reagents. The use of netal exchange reagents has been employed in lieu of the ashing step to
liberate lead from binding sites, although this substitution is associated with less
precision. For the ashing method, relative precision 1s approximately 5 percent. In terms of
accuracy and sensitivity, 1t appears that there are problems at low levels, e.g., 5 pg/dl or
below, particularly 1f samples contain elevated cooper levels.
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Lead in Plasma. Since lead in whole blood is virtually all confined to the erythrocyte,
plasma levels are quite low and it appears that extreme care must be employed to reliably
measure plasma levels. The best method for such measurement is IDMS, in tandem with ultra-
clean facility use. Atonic absorption spectrometry is satisfactory for comparative analyses
across a range of relatively high whole blood values.
Lead in Teeth. Lead measurement in teeth has involved either whole tooth sampling or
analysis of specific regions, such as primary or circumpulpal dentine. In either case, sam-
ples must be solublized after careful surface cleaning to remove contamination; solubilization
is usually accompanied by either wet ashing directly or ashing subsequent to a dry ashing
step.
Atomic absorption spectrometry and anodic stripping have been employed more frequently
for such determinations than any other method. With AAS, the high mineral content of teeth
argues for preliminary isolation of lead via chelation-extraction. The relative precision of
analysis for within-run measurement is around 5-7 percent, with the main determinant of vari-
ance in regional assay being the initial Isolation step. One change from the usual methods
for such measurement is the in situ measurement of lead by X-ray fluorescence spectrometry in
children. Lead measured in this fashion allows observation of on-going lead accumulation,
rather than waiting for exfoliation.
Lead in Hair. Hair as an exposure Indicator for lead offers the advantages of being non-
invasive and a medium of indefinite stability. However, there is still the crucial problem of
external surface contamination, which is such that it is still not possible to state that any
cleaning protocol reliably differentiates between external and Internally deposited lead.
Studies that demonstrate a correlation between increasing hair lead and increasing sever-
ity of a measured effect probably support arguments for hair being an external indicator of
exposure. It is probably also the case, then, that such measurement, using cleaning protocols
that have not been independently validated, will overstate the relative accumulation of "in-
ternal" hair lead 1n terms of some endpoint and will also underestimate the relative sensiti-
vity of changes in internal lead content with exposure. One consequence of this would be, for
example, an apparent threshold for a given effect in terms of hair lead which 1s significantly
above the actual threshold. Because of these concerns, hair 1s best used with the simultan-
eous measurement of blood lead.
Lead in Urine. Analysis of lead in urine Is complicated by the relatively low levels of
the element in this medium as well as the complex mixture of mineral elements present. Urine
lead levels are most useful and also somewhat easier to determine in cases of chelation mobil-
ization or chelation therapy, where levels are high enough to permit good precision and dilu-
tion of matrix interference.
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Samples are probably best analyzed by prior chemical wet ashing, using the usual mixture
of acids. Both anodic stripping voltammetry and atomic absorption spectrometry have been
applied to urine analysis, with the latter more routinely used and usually with a chelation/
extraction step.
Lead in Other Tissues. Bone samples require cleaning procedures for removal of muscle
and connective tissue and chemical solubilization prior to analysis. Methods of analysis are
comparatively limited and it appears that flameless atomic absorption spectrometry is the
technique of choice.
Lead measurements in bone, in vivo, have been reported with lead workers, using X-ray
fluorescence analysis and a radioisotopic source for excitation. One problem with this
approach with moderate lead exposure is the detection limit, approximately 20 ppm. Soft organ
analysis poses a problem in terms of heterogeneity in lead distribution within an organ (e.g.,
brain and kidney. In such cases, regional sampling or homogenization must be carried out.
Both flame and flameless atomic absorption spectrometry appear to be satisfactory for soft
tissue analysis and are the most widely used.
Quality Assurance Procedures in Lead Analyses. In terms of available information, the
major focus in establishing quality control protocols for lead has involved whole blood meas-
urements. Translated into practice, quality control revolves around steps employed within the
laboratory, using a variety of internal checks, and the further reliance on external checks,
such as a formal continuing multi-laboratory proficiency testing program.
Within the laboratory, quality assurance protocols can be divided into start-up and rou-
tine procedures, the former involving establishment of detection limits, within-run and
between-run precision, analytical recovery, and comparison with some reference technique
within or outside the laboratory. The reference method is assumed to be accurate for the par-
ticular level of lead in some matrix at a particular point in time. Correlation with such a
method at a satisfactory level, however, may simply indicate that both methods are equally
inaccurate but performing with the same level of precision proficiency. More preferable is
the use of certified samples having lead at a level established by the definitive method.
For blood lead, the Centers for Disease Control periodically survey overall accuracy and
precision of methods used by reporting laboratories. In terms of overall accuracy and preci-
sion, one such survey found that anodic stripping voltammetry as well as the Delves cup and
extraction variations of atomic absorption spectrometry performed better than other proce-
dures. These results do not mean that a given laboratory cannot perform better with a partic-
ular technique; rather, such data are of assistance for new facilities choosing among methods.
Of particular value to laboratories carrying out blood lead analysis are the external
quality assurance programs at both the state and federal levels. The most comprehensive
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proficiency testing program is that carried out by the Centers for Disease Control, USPHS.
This program actually consists of two subprograms, one directed at facilities involved in lead
poisoning prevention and screening (Center for Environmental Health) and the other concerned
with laboratories seeking certification under the Clinical Laboratories Improvement Act of
1967 as well as under regulations of the Occupational Safety and Health Administration's
(OSHA) Laboratory Improvement Program Office. Overall, the proficiency testing programs have
served their purpose well, judging from the relative overall improvements In reporting
laboratories over the years of the programs' existence. In this regard, OSHA criteria for
laboratory certification require 8 of 9 samples be correctly analyzed for the previous
quarter. This level of required proficiency reflects the ability of a number of laboratories
to actually perform at this level.
9.8.2 Determination of Erythrocyte Porphyrin (Free Erythrocyte Protoporphyrin, Zinc
Protoporphyrin)
With lead exposure, there is an accumulation of erythrocyte protoporphyrin IK, owing to
Impaired placement of divalent iron to form heme. Divalent zinc occupies the place of the na-
tive iron. Depending upon the method of analysis, either metal-free erythrocyte porphyrin or
zinc protoporphyrin (ZPP) is measured, the former arising from loss of zinc in the chemical
manipulation. Virtually all methods now in use for EP analysis exploit the ability of the
porphyrin to undergo intense fluorescence when excited by ultraviolet light. Such fluoro-
metric methods can be further classified as wet chemical micromethods or direct measuring
fluorometry using the hematofluorometer. Owing to the high sensitivity of such measurement,
relatively small blood samples are required, with liquid samples or blood collected on filter
paper.
The most common laboratory or wet chemical procedures now in use represent variations of
several common chemical procedures: 1) treatment of blood samples with a mixture of ethyl
acetate/acetic acid followed by a repartitioning into an inorganic acid medium, or 2) solu-
bilization of a blood sample directly into a detergent/buffer solution at a high dilution.
Quantification has been done using protoporphyrin, coproporphyria or zinc protoporphyrin IX
plus pure zinc ion. The levels of precision for these laboratory techniques vary somewhat
with the specifics of analysis. The Piomelli method has a coefficient of variation of 5
percent, while the direct ZPP method using buffered detergent solution is higher and more
variable.
The recent development of the hematofluorometer has made it possible to carry out EP
measurements in high numbers, thereby making population screening feasible. Absolute calibra-
tion is necessary and requires periodic adjustment of the system using known concentrations of
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EP In reference blood samples. Since these units are designed for oxygenated blood, i.e.,
capillary blood, use of venous blood requires an oxygenation step, usually a moderate shaking
for several minutes. Measurement of low or moderate levels of EP can be affected by interfer-
ence with bilirubin. Competently employed, the hematofluorometer appears to be reasonably
precise, showing a total coefficient of variation of 4.11-11.5 percent. While the comparative
accuracy of the unit has been reported to be good relative to the reference wet chemical tech-
nique, a very recent study has shown that commercial units carry with them a significant nega-
tive bias, which may lead to false negatives in subjects having only moderate EP elevation.
Such a bias in accuracy has been difficult to detect in existing EP proficiency testing
programs. It appears that, by comparision to wet methods, the hematofluorometer should be
restricted to field use rather than becoming a substitute in the laboratory for chemical meas-
urement, and field use should involve periodic split-sample comparison testing with the wet
method.
9.8.3 Measurement of Urinary Coproporphyria
Although EP measurement has largely supplanted the use of urinary coproporphyrin analysis
(CP-U) to monitor excessive lead exposure in humans, this measurement is still of value in
that it reflects active intoxication. The standard analysis is a fluorometric technique,
whereby urine samples are treated with buffer, and an oxidant (Iodine) is added to generate CP
from its precursor. The CP-U is then partitioned into ethyl acetate and re-extracted with
dilute hydrochloric acid. The working curve is linear below 5 Mi CP/dl urine.
9.8.4 Measurement of Delta-Aminolevulinic Acid Dehydrase Activity
Inhibition of the activity of the erythrocyte enzyme, delta-aminolevulinic acid dehydra-
tase (AlA-D), by lead is the basis for using such activity in screening for excessive lead
exposure. A number of sampling and sample handling precautions attend such analysis. Since
zinc (II) ion will offset the degree of activity inhibition by lead, blood collecting tubes
must have extremely low zinc content. This essentially rules out the use of rubber-stoppered
blood tubes. Enzyme stability is such that the activity measurement is best carried out
within 24 hours of blood collection. Porphobilinogen, the product of enzyme action, is light-
labile and requires the assay be done in restricted light. Various procedures for ALA-D meas-
urement are based on measurement of the level of the chromophorlc pyrrole (approximately
555 mi) formed by condensation of the porphobilinogen with p-dimethylaminobenzaldehyde.
In the European Standardized Method for ALA-D activity determination, blood samples are
hemolyzed with water, ALA solution added, followed by incubation at 37°C, and the reaction
terminated by a solution of mercury (II) in trichloroacetic acid. Filtrates are treated with
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modified Ehrlich's reagent (p-dimethyl aminobenzaldehyde) in trichloroacetic/perchloroacetic
acid mixture. Activity is quantified in terms of micromoles ALA/nin/liter erythrocytes.
One variation in the above procedure is the initial use of a thiol agent, such as dithio-
threotol, to reactivate the enzyme, giving a measure of the full native activity of the
enzyme. The ratio of activated/unactivated activity vs. blood lead levels accomodates genetic
differences between individuals.
9.8.5 Measurement of Delta-Aminolevulinic Acid in Urine and Other Media
Levels of delta-aminolevulinic acid (6-ALA) in urine and plasma increase with elevated
lead exposure. Thus, measurement of this metabolite, generally in urine, provides an index of
the level of lead exposure. ALA content of urine samples (ALA-U) is stable for about two
weeks or more with sample acidification and refrigeration. Levels of ALA-U are adjusted for
urine density or expressed per unit creatinine. If feasible, 24-hour collection is more
desirable than spot sampling.
Virtually all the various procedures for ALA-U measurement employ preliminary isolation
of ALA from the balance of urine constituents. In one method, further separation of ALA from
the metabolite aminoacetone is done. Aminoacetone can interfere with colorimetric measure-
ment. ALA is recovered, condensed with a beta-dicarbonyl compound, e.g., acetyl acetone, to
yield a pyrrole intermediate. This intermediate is then reacted with p-dimethylamino-
benzaldehyde in perchloric/acetic acid, followed by colorimetric reading at 553 nm. In one
variation of the basic methodology, ALA is condensed with ethyl acetoacetate directly and the
resulting pyrrole extracted with ethyl acetate. Ehrlich's reagent is then added as in other
procedures and the resulting chromophore measured spectrophotometrically.
Measurement of ALA in plasma is much more difficult than 1n urine, since plasma ALA is at
nanogram/milliter levels. In one gas-liquid chromatographic procedure, ALA is isolated from
plasma, reacted with acetyl acetone and partitioned into a solvent that also serves for
pyrolytic methylation of the involatile pyrrole in the injector port of the chromatograph,
making the derivative more volatile. For quantification, an interval standard, 6-am1no-5-
oxohexanoic acid, is used. While the method is more involved, it is more specific than the
older colorimetric technique.
9.8.6 Measurement of Pyrimidine-5'-Nucleotidase Activity
Erythrocyte pyr1m1dine-5'-nucleotidase (Py5N) activity Is inhibited with lead exposure.
Presently two different methods are used for assaying the activity of this enzyme. The older
method is quite laborious in time and effort, whereas the more recent approach is shorter but
uses radioisotopes and radiometric measurement.
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In the older method, heparinized venous blood is filtered through cellulose to separate
erythrocytes from platelets and leukocytes. Cells are then freeze-fractured and the hemo-
lysates dialyzed to remove nucleotides and other phosphates. This dlalysate Is then incubated
1n the presence of a nucleoside monophosphate and cofactors, the enzyme reaction being termi-
nated by treatment with trichloroacetic acid. The inorganic phosphate isolated from added
substrate is measured colorlmetrically as the phosphomolybdlc acid complex.
In the radiometric assay, hemolysates obtained as before are incubated with pure 14C-CMP.
By addition of a barium hydroxide/zinc sulfate solution, proteins and unreacted nucleotide are
precipitated, leaving labeled cytidine In the supernatant. Aliquots are measured for 14C ac-
tivity In a liquid scintillation counter. This method shows a good correlation with the ear-
lier technique.
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10. METABOLISM OF LEAD
10.1 INTRODUCTION
The absorption, distribution, retention, and excretion of lead in humans and animals as
well as the various factors that mediate the extent of toxicokinetic processes are discussed
in this chapter. While inorganic lead is the form of the element that has been most heavily
studied, organolead compounds are also emitted into the environment and, as they are quite
toxic, they are also included in the-tliseussion. Since the preparation of the 1977 Air
Quality Criteria Document for Lead (U.S. Environmental Protection Agency, 1977), a number of
reports have appeared that have proved particularly helpful in both quantifying the various
processes to be discussed in this chapter and assessing the interactive impact of factors such
as nutritional status in determining internal exposure risk.
10.2 LEAD ABSORPTION IN HUMANS AND ANIMALS
The amounts of lead entering the bloodstream from various routes of absorption are deter-
mined not only by the levels of the element in the particular media, but also by the various
physical and chemical parameters that characterize lead. Furthermore, specific host factors,
such as age and nutritional status, are important, as is Interindividual variability. Addi-
tionally, in order to assess absorption rates, it is necessary to know whether or not the sub-
ject is in "equilibrium" with respect to a given level of lead exposure.
10.2.1 Respiratory Absorption of Lead
The movement of lead from ambient air to the bloodstream is a two-part process: a frac-
tion of air lead 1s deposited in the respiratory tract and, of this deposited amount, some
fraction is subsequently absorbed directly into the bloodstream or otherwise cleared from the
respiratory tract. At present, enough data exist to make some quantitative statements about
both of these components of respiratory absorption of lead.
The 1977 Air Quality Criteria Document for Lead described the model of the International
Radiological Protection Commission (IRPC) for the deposition and removal of lead from the
lungs and the upper respiratory tract (International Radiological Protection Commission,
1966). Briefly, the model predicts that 35 percent of lead inhaled from ambient air is depos-
ited in the airways, with most of this going to the lung. The IRPC model predicts a total de-
position of 40-50 percent for particles with an aerodynamic diameter of 0.5 pm and indicates
that the absorption rate would vary, depending on the solubility of the particular form.
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PRELIMINARY DRAFT
10.2.1.1 Human Studies. Table 10-1 tabulates the various studies of human subjects that pro-
vide data on the deposition of inorganic lead in the respiratory tract. Studies of this type
have involved diverse methodology to characterize the inhaled particles in terms of both size
(and size ranges) and fractional distribution. The use of radioisotopic or stable lead iso-
topes to directly or indirectly measure lead deposition and uptake into the bloodstream has
been particularly helpful in quantifying these processes.
From the studies of Kehoe (1961a,b,c) and their update by Gross (1981) as well as data
from Chamberlain et al. (1978), Morrow et al. (1980), and Nozaki (1966), it appears that the
respiratory deposition of airborne lead as encountered in the general population is approx-
imately 30-50 percent, depending on particle size and ventilation rates. Ventilation rate is
particularly important with submicron particles, where Brownian diffusion governs deposition,
since a slower breathing rate enhances the frequency of collisions of particles with the alve-
olar wall.
Figure 10-1 reproduces a composite figure of Chamberlain et al. (1978) that compares
data, both calculated and experimentally measured, on the relationship of percentage deposi-
tion to particle size. • With increasing particle size, deposition rate decreases to a minimum
over the range where Brownian diffusion predominates, followed by an Increase in deposition
with size (>0.5 pm MMAO) as impaction and sedimentation become the main deposition factors.
In contrast to the ambient air or chamber data tabulated in Table 10-1, higher deposition
rates in some occupational settings are associated with relatively large particles. However,
much of this deposition will be in the upper respiratory tract, with eventual movement to the
gastrointestinal tract by ciliary action and swallowing. Mehani et al. (1966) measured depo-
sition rates in battery workers and workers in marine scrap yards and observed total depositon
rates of 28-70 percent. Chamberlain and Heard (1981) calculated an absorption rate for parti-
cle sizes encountered in workplace air of appproximately 47 percent.
Systemic absorption of lead from the lower respiratory tract occurs directly, while much
of the absorption from the upper tract involves swallowing and some uptake in the gut. From
the radioactive isotope data of Chamberlain et al. (1978) and Morrow et al. (1980), and the
stable isotope studies of Rabinowitz et al. (1977), it can be concluded that lead deposited in
the lower respiratory tract is quantitatively absorbed.
Chamberlain et al. (1978) used 203Pb-labeled lead in engine exhaust, lead oxide, or lead
nitrate aerosols in experiments where human subjects inhaled the lead from a chamber through a
mouthpiece or in wind tunnel aerosols. By 14 days, approximately 90 percent of the label was
removed from the lung. Lead movement Into the bloodstream could not be described by a simple
exponential function; 20 percent was absorbed within 1 hour and 70 percent within 10 hours.
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TABLE 10-1. DEPOSITION OF LEAD IN THE HUMAN RESPIRATORY TRACT
Form
Particle
size
Exposure
Percent
deposition
Reference
Pb203 aerosols
from engine«
exhaust
0.05 pin median
count diameter
in 38 studies;
5 subjects
exposed to average
of 0.9 pro
Lead "fumes" 0.05-1.0 pm mean
made in indue- diameter
tion furnace
203Pb-labeled
Pbz03 aerosol
Ambient air
lead near
motorway and
other urban
areas in U.K.
203pb-labeled
Pb(0H)2 or
PbCl2 aero-
sols
Lead in work-
place air;
battery
factory and
shipbreaking
operations
Dean densities
of 0.02, 0.04,
0.09 pm
Mainly 0.1 pm
Both forms at
0.25 pm MMAD
Not determined;
defined as fumes,
fine dust, or
coarse dust
Chamber studies; 10, 20,
or 150 pg/m3; 3 hr on
alternate days;
12 subjects
Mouthpiece/aerosol chamber;
10 mg/m3; adult subjects
Mouthpiece/aerosol chamber;
adult subjects
2-10 pg/m3; adult subjects
50 liters air; 0.2 pCi/
liter; adult subjects
3 adult groups:
23 pg/m3 - controls
86 pg/m3 - battery workers
180 pg/m3 - scrap yard
30-70* (mean: 48%)
for mainly
0.05 pm particles
42% 0.05 pm;
63% 1.0 pm
80% 0.02 pni;
45% 0.04 ym
30% 0.09 pi?
60%, fresh exhaust;
50% other urban
area
23%, chloride;
26%, hydroxide
47%, battery workers;
39%, shipyard and
controls
Kehoe, 1961a,b,c;
Gross, 1981
Nozaki, 1966
Chamberlain et al.,
1978
Chamberlain et al.,
1978
Morrow et al., 1980
Mehani, 1966
-------
PRELIMINARY DRAFT
80
70
O
z
3
_j
Z 60
O
tn
s
Ui
O
u
z
IU
u
ee
UI
0.
BO
40
30
20
10
n i i
(?) »»Pb DATA (VT = 1000 cm*)
(2) HEYOER 1975 (VT= 1000 cm')
(5) MITCHELL 1977 (VT = 1000 cm1}
(T) JAMES 1978 (VT = 1000 cm1) CALCULATED -
(?) JAMES 1878 iVj = 500 cm') CALCULATED
(?) YU 1977 (VT = cm') CALCUATED
BREATHING CYCLE 4 SECONDS
0.01
D MED
DIFFUSION MEAN
EQUIVALENT OIA.
0.1 |4m
M MED
MASS MEDIAN
EQUIV. DIA.
Figure 10-1. Effect of particle size on lead deposition rate in the lung.
Source: Chamberlain et al. (1978).
1.0
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PRELIMINARY DRAFT
Rabinowltz et al. (1977) administered 20
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PRELIMINARY DRAFT
Boudene et al. (1977) exposed rats to 210Pb-labeled aerosols at a level of 1 label/m3
and 10 pg/m3, the majority of the particles being 0.1-0.5 pm in size. At 1 hour, 30 percent
of the label had left the lung; by 48 hours 90 percent was gone.
Bianco et al. (1974) used 2l2Pb aerosol (SO.2 pm) inhaled briefly by dogs and found a
clearance half-time from the lung of approximately 14 hours. Greenhalgh et al. (1979) found
that direct instillation of 203Pb-labeled lead nitrate solution into the lungs of rats led to
an uptake of approximately 42 percent within 30 minutes, compared with an uptake rate of 15
percent within 15 minutes in the rabbit. These instillation data are consistent with the
report of Pott and Brockhaus (1971), who noted that intratracheal instillation of lead in
solution (as bromide) or suspension (as oxide) serially over 8 days resulted in systemic lead
levels in tissues indistinguishable from injected lead. Rendal1 et al. (1975) found that the
movement of lead into blood of baboons inhaling a lead oxide (Pb304) was more rapid and
resulted in higher levels when coarse (1.6 pm mean diameter) rather than fine (0.8 pm mean
diameter) particles were used. This suggests that considerable fractions of both size parti-
cles were eventually lodged in the gut, where absorption of lead tends to be higher in baboons
than in other animal species (Pounds et al., 1978). In addition, the larger particles appear
to move more rapidly to the gut.
10.2.2 Gastrointestinal Absorption of Lead
Gastrointestinal absorption of lead mainly involves uptake from food and beverages as
well as lead deposited in the upper respiratory tract and eventually swallowed. It also in-
cludes ingestion of non-food material, primarily in children via normal mouthing activity and
pica. Two issues of concern with lead uptake from the gut are the comparative rates of such
absorption in developing vs. adult organisms, including humans, and how the bioavailability of
lead affects such uptake.
10.2.2.1 Human Studies. Based on the long-term metabolic studies with adult volunteers,
Kehoe (1961a,b,c) estimated that approximately 10 percent of dietary lead is absorbed from the
gut of humans. According to Gross (1981), there can be considerable variation of various
balance parameters among subjects. These studies did not take into account the contribution
of biliary clearance of lead into the gut, which would have affected measurements for both
absorption and total excretion. Chamberlain et al. (1978) also determined that the level of
endogenous fecal lead is approximately 50 percent of urinary lead values. Chamberlain et al.
(1978) have estimated that 15 percent of dietary lead is absorbed, if the amount of endogenous
fecal lead 1s taken into account.
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PRELIMINARY ORAFT
(range 5-17); the mean absorption rate determined from netabolic balance studies was 53 per-
cent. Ziegler et al. (1978) carried out a total of 89 netabolic balance studies with 12 nor-
aal infants aged 2 weeks to 2 years. Diets were closely controlled and lead content was
measured. Two discrete studies were carried out and in the first, 51 balance studies using 9
children furnished a Mean absorption rate of 42.7 percent. In the second study, 6 children
were involved in 38 balance studies involving dietary lead intake at 3 levels. For all daily
intakes of 5 Mi Pb/kg/day or higher, the mean absorption rate was 42 percent. At low levels
of lead intake data were variable, with some children apparently in negative balance, probably
due to the difficulty in controlling low lead Intake.
In contrast to these studies, Barltrop and Strehlow (1978) found that with children hos-
pitalized as orthopedic or "social" admissions, the results were highly variable. A total of
104 balance studies were carried out in 29 children ranging in age from 3 weeks to 14 years.
Fifteen of the subjects were in net negative balance, with an average dietary absorption of
-40 percent and, when weighted by number of balance studies, -16 percent.
It is difficult to closely compare these data with those of Ziegler et al. (1978). Sub-
jects were inpatients, represented a nuch greater age range, and were not classified in terms
of mineral nutrition or weight change status. As an urban pediatric group, the children in
this study may have had higher prior lead exposure so that the "washout" phenomenon (Kehoe,
1961a,b,c; Gross, 1981) may have contributed to the highly variable results. The calculated
mean daily lead intake in the Barltrop and Strehlow group (6.5 MSj/kfl/day) was lower than those
for all but one study group described by Ziegler et al. (1978). In the latter study it ap-
pears that data for absorption became more variable as the daily lead Intake was lowered.
Finally, In those children classified as orthopedic admissions, it is not clear that skeletal
trauma was without effect on lead equilibrium between bone and other body compartments.
As typified by the results of the NHANES II survey (Mahaffey et al., 1979), children at
2-3 years of age show a small peak in blood lead during childhood. The question arises
whether this peak indicates an intrinsic biological factor, such as increased absorption or
retention when compared with older children, or whether this age group is exposed to lead in
some special way. Several studies are relevant to the question. Zielhuis et al. (1978) re-
ported data for blood lead levels 1n 48 hospitalized Dutch children ranging in age from 2
months to 6 years. Children up to 3 years old had a mean blood lead level of 11.9 vs. a
level of 15.5 In children aged 4-6 years. A significant positive relationship between child
age and blood lead was calculated (r = 0.44, p <0.05). In the Danish survey by Nygaard et al.
(1977), a subset of 126 children representing various geographical areas and age groups
yielded the following blood lead values by mean age group: children (N = 8) with a mean age of
1.8 years had a mean blood lead of 4.3 pg/dl; those with a mean age of 3.7-3.9 had values
ranging from 5.6 to 8.3 pg/dl children 4.6-4.8 years of age had a range of 9.2 to 10 Mfl/dl.
NEW10A/A 10-8 7/1/83
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PRELIMINARY DRAFT
Following the Kehoe studies, a nunber of reports determined gastrointestinal (GI) absorp-
tion using both stable and radioisotopic labeling of dietary lead. Generally, these reports
support the observation that in the adult human there is limited absorption of lead when taken
with food. Harrison et al. (1969) determined a mean absorption rate of 14 percent for three
adult subjects ingesting 203Pb-labeled lead in diet, a figure in accord with the results of
Hursh and Suomela (1968). Chamberlain et al. (1978) studied the absorption of 203Pb in two
forms (as the chloride and as the sulfide) taken with food. The corresponding absorption
rates were 6 percent (sulfide) and 7 percent (chloride), taking into account endogenous fecal
excretion. Using adult subjects who ingested the stable isotope 204Pb in their diet,
Rabinowitz et al. (1974) reported an average gut absorption of 7.7 percent. In a later study,
Rabinowitz et al. (1980) measured an absorption rate of 10.3 percent.
A number of recent studies indicate that lead ingested under fasting conditions is absor-
bed to a much greater extent than when It 1s taken with or incorporated Into food. For exam-
ple, Blake (1976) measured a mean absorption rate of 21 percent when 11 adult subjects in-
gested 203Pb-labeled lead chloride several hours after breakfast. Chamberlain et al. (1978)
found that lead uptake in six subjects fed 203Pb as the chloride was 45 percent after a fast-
ing period, compared to 6 percent with food. Heard and Chamberlain (1982) obtained a rate of
63.3 percent using a similar procedure with eight subjects. Rabinowitz et al. (1980) reported
an absorption rate of 35 percent in five subjects when 204Pb was ingested after 16 hours of
fasting. To the extent that lead in beverages is ingested between meals, these isotope
studies support the observations of Barltrop (1975) and Garber and Wei (1974) that beverage
lead is absorbed to a greater extent than is lead in food.
The relationship of lead bioavailability in the human gut to the chemical/biochemical
form of lead can be determined from available data, although interpretation is complicated by
the relatively small amounts given and the presence of various components of food already pre-
sent in the gut. Harrison et al, (1969) found no difference in lead absorption from the human
gut when lead isotope was given either as the chloride or incorporated into alginate. Cham-
berlain et al. (1978) found that labeled lead as the chloride or sulfide was absorbed to the
same extent when given with food,( while the sulfide form was absorbed at a rate of 12 percent
compared with 45 percent for the chloride when given under fasting conditions. Rabinowitz et
al. (1980) obtained similar absorption rates for the chloride, sulfide, or cysteine complex
forms when administered with food or under fasting conditions. Heard and Chamberlain (1982)
found no difference in absorption rate when isotopic lead (!03Pb) was given with unlabeled
liver and kidney or when the label was first incorporated into these organs.
Three studies have focused on the question of differences in gastrointestinal absorption
rates between adults and children. Alexander et al. (1973) carried out 11 balance studies
with 8 children, aged 3 months to 8 years. Intake averaged 10.6 pg Pb/kg body weight/day
NEW10A/A 10-7 7/1/83
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PRELIMINARY DRAFT
10.2.2.2 Animal Studies. Lead absorption via the gut of various adult experimental animal
species appears to resemble that for the adult human, on the order of 1-15 percent in most
cases. Kostlal and Kello (1979), Kostlal et al. (1978), and Kostial et al. (1971) reported a
value of 1 percent or less in adult rats maintained on commercial rat chow. These studies
were carried out using radioisotopic tracers. Similarly, Barltrop and Meek (1975) reported an
absorption rate of 4 percent in control diets, while Aungst et al. (1981) found the value to
range from 0.9 to 6.9 percent, depending on the level of lead given in the diet. In these rat
studies, lead was given with food. Quarterman and Morrison (1978) administered 203Pb label in
small amounts of food to adult rats and found an uptake rate of approximately 2 percent at 4
months of age. Pounds et al. (1978) obtained a value of 26.4 percent with four adult Rhesus
monkeys given 210Pb by gastric intubation. The higher rate, relative to the rat, may reflect
various states of fasting at time of intubation or differences in dietary composition (vide
infra), two factors that affect rates of absorption.
As seen above with human subjects, fasting appears to enhance the rate of lead uptake in
experimental animals. Garber and Wei (1974) found that fasting markedly enhanced gut uptake
of lead in rats. Forbes and Reina (1972) found that lead dosing by gastric intubation of rats
yielded an absorption rate of 16 percent, which is higher than other data for the rat. It is
likely that intubation was done when there was little food in the gut. The data of Pounds et
al. (1978), as described above, may also suggest a problem with giving lead by gastric intuba-
tion or with water as opposed to mixing it with food.
The bioavailability of lead in the gastrointestinal tract of experimental animals has
been the subject of a number of reports. The designs of these studies differed in accordance
with how "bioavailability" is defined by different investigators. In some cases, the dietary
matrix was kept constant, or nearly so, while the chemical or physical form of the lead was
varied. By contrast, other data described the effect of changes in bioavailability as the
basic diet matrix was changed. The latter case is complicated by the simultaneous operation
of lead-nutrient interactive relationships, which are described in Section 10.5.2 within this
chapter.
Allcroft (1950) observed comparable effects when calves were fed lead in the form of the
phosphate, oxide, or basic carbonate (PbC03-Pb(0H)2), or incorporated into wet or dry paint.
By contrast, lead sulfide in the form of finely ground galena ore was less toxic. Criteria
for relative effect included kidney and blood lead levels and survival rate over time.
In the rat, Barltrop and Meek (1975) carried out a comparative absorption study using
lead in the form of the acetate as the reference substance. The carbonate and thai!ate were
absorbed to the greatest extent, while absorption of the sulfide, chromate, napthenate, and
octoate was 44-67 percent of the reference agent. Gage and Litchfield (1968, 1969) found
that lead napthenate and chromate can undergo considerable absorption from the rat gut when
NEW10A/A 10-10 7/1/83
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PRELIMINARY DRAFT
incorporated into dried paint films, although less than when given with other vehicles. Ku et
al. (1978) found that lead in the form of the acetate or as a phospholipid complex was equally
absorbed from the 61 tract of both adult and young rats at a level of 300 ppm. Uptake was
assessed by weight change, tissue levels of lead, and urinary aminolevulinic acid levels.
In a study relevant to the problem of lead bioavailability in soils and dusts, particu-
larly in exposed children, Dacre and Ter Haar (1977) compared the effects of lead as acetate
with lead contained in roadside soil and in house paint soil, at a level of approximately 50
ppm, in commercial rat chow. Uptake of lead was indexed by weight change, tissue lead con-
tent, and inhibition of ALA-D activity. There was no significant difference in any of these
parameters across the three groups, suggesting that neither the geochemical matrix in the
soils or the various chemical forms—basic carbonate in paint soil, and the oxide, carbonate,
and basic carbonate in roadside soi 1—affect lead uptake.
These data are consistent with the behavior of lead in dusts upon acid extraction as re-
ported by Day et al. (1979), Harrison (1979), and Duggan and Williams (1977). In the Day et
al. study, street dust samples from England and New Zealand were extracted with hydrochloric
acid over the pH range of 0-5. At an acidity that may be equalled by gastric secretions,
i.e., pH of 1, approximately 90 percent of the dust lead was solubilized, Harrison (1979)
noted that at this same acidity, up to 77 percent of Lancaster, England, street dust lead was
soluble, while an average 60 percent solubility was seen in London dust samples (Duggan and
Williams, 1977). Because gastric solubilization must occur for lead in these media to be ab-
sorbed, the above data are useful in determining relative risk. - ' . •.
Kostial and Kello (1979) compared the absorption of 203Pb from the gut of rats maintained
on commercial rat chow vs. rats fed such "human" diets as baby foods, porcine liver, bread,
and cow's milk. Absorption in the latter cases varied from 3 to 20 percent, compared with
<1.0 percent with rat chow. This range of uptake for the non-chow diet compares closely with
that reported for human subjects (vide supra). Similarly, Jugo etral. -(1975a) observed that
rats maintained on fruit diets had an absorption rate of 18-20 percent. It would appear,
then, that the generally observed lower absorption of lead in the adult rat vs. the adult
human is less reflective of a species difference than of a dietary difference.
Barltrop and Meek (1979) studied the relationship of particle size of lead in two
forms--as the metal or as lead octoate or chromate in powdered paint films—to the amount of
gut absorption in the rat and found that there was an inverse relationship between uptake and
particle size for both forms.
A number of studies have documented that the developing animal absorbs a relatively
greater fraction of ingested lead than does the adult, thus supporting those studies that have
shown this age dependency in humans. For example, the adult rat absorbs approximately 1 per-
cent lead or less when contained in diet vs. a corresponding value 40-50 times greater in the
NEW10A/A 10-11 7/1/83
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PRELIMINARY DRAFT
rat pup (Kostlal et al., 1971, 1978;, Forbes and Reina, 1972). In the rat, this difference
persists through weaning (Forbes and Reina, 1972), at which point uptake resembles that of
adults. Part of this difference can be ascribed to the nature of the diet (Bother's milk vs.
regular diet), although it should be noted that the extent of absorption enhancement with milk
vs. rat chow In the adult rat (Kello and Kostial, 1973) falls short of what is seen in the
neonate. An undeveloped, less selective intestinal barrier may also exist in the rat neonate.
In non-human primates, Munro et al. (1975) observed that infant monkeys absorbed 65-85 percent
via the gut vs. 4 percent in adults. Similarly, Pounds et al. (1978) noted that juvenile
Rhesus monkeys absorbed approximately 50 percent more lead than adults.
The question of the relationship of level of lead intake through the GI tract and rate of
lead absorption was addressed by Aungst et al. (1981), who exposed adult and suckling rats to
doses of lead by intubation over the range 1-100 mg Pb/kg or by variable concentrations in
drinking water. With both age groups and both forms of oral exposure, lead absorption as a
percentage of dose decreased, suggesting a saturation phenomenon for lead transport across the
gut wall.
10.2.3 Percutaneous Absorption of Lead
Absorption of inorganic lead compounds through the skin appears to be considerably less
significant than the respiratory and gastrointestinal routes of uptake. This is in contrast
to the .observations for lead alKyls and other organic derivatives (U.S. Environmental
Protection Agency, 1977). Uptake of alkyl lead through the skin is discussed in Section 10.7.
Rastogi and Clausen (1976) found that cutaneous or subcutaneous administration of lead
napthenate in rat skin was associated with higher tissue levels and more severe toxic effects
than was the case for lead acetate. Laug and Kunze (1948) applied lead as the acetate, ortho-
arsenate, oleate, and ethyl lead to rat skin and determined that the greatest levels of kidney
lead were associated with the alkyl contact.
Moore et al. (1980) studied the percutaneous absorption of 203Pb-labeled lead acetate in
cosmetic preparations using eight adult volunteers. Applied in wet or dry forms, absorption
was indexed by blood, urine, and whole body counting. Absorption rates ranged from 0 to 0.3
percent, with the highest values obtained when the application sites were scratched. These
researchers estimated that the normal use of such preparations would result in an absorption
of approximately 0.06 percent.
10.2.4 Transplacental Transfer of Lead
Lead uptake by the human and animal fetus occurs readily, based on such indices as fetal
tissue lead measurements and, in the human, cord blood lead levels. Barltrop (1969) and
Horiuchi et al. (1959) demonstrated by fetal tissue analysis that placental transfer in the
NEW10A/A 10-12 7/1/83
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PRELIMINARY DRAFT
human occurs by the 12th week of gestation, with increasing fetal lead uptake throughout deve-
lopment. Highest levels occur in bone, kidney, and liver, followed by blood, brain, and
heart. Cord blood contains significant amounts of lead, generally correlating with maternal
blood values and being slightly but significantly lower than mothers' in concentration
(Scanlon, 1971; Harris and Hoi ley, 1972; Gershanik et al. , 1974; Buchet et al. , 1978;
Alexander and Delves, 1981; Rabinowitz and Needleman, 1982).
A cross-sectional study of maternal blood lead carried out by Alexander and Delves (1981)
showed that a significant decrease in maternal blood lead occurs throughout pregnancy, a de-
crease greater than the dilution efffect of the concurrent increase in plasma volume. Hence,
during pregnancy there is either an increasing deposition of lead in placental or fetal tissue
or an increased loss of body lead via other routes. Increasing absorption by the fetus during
gestation, as demonstrated by Barltrop (1969), suggests that the former explanation is a
likely one. Hunter (1978) found that summer-born children showed a trend to higher blood lead
than those born in the spring, suggesting increased fetal uptake in the summer due to in-
creases in circulating maternal lead. This observation was confirmed in the report of
Rabinowitz and Needleman (1982). Ryu et al. (1978) and Singh et al. (1978) both reported that
infants born to women having a history of lead exposure had significantly elevated blood lead
values at birth
10.3 DISTRIBUTION OF LEAD IN HUMANS AND ANIMALS
A quantitative understanding of the sequence of changes in levels of lead In various body
pools and tissues is essential in interpreting measured levels of lead with respect to past
exposure as well as present and future risks of toxicity. This section discusses the dis-
tribution kinetics of lead in various portions of the body—blood, soft tissues, calcified
tissues, and the "chelatable" or toxicologically active body burden--as a function of such
parameters as exposure history and age.
A given quantity of lead taken up from the GI tract or the respiratory tract into the
bloodstream is initially distributed according to the rate of delivery by blood to the various
organs and systems. Lead is then redistributed to organs and systems in proportion to their
respective affinities for the element. With consistent exposure for an extended period, a
near steady-state of intercompartmental distribution is achieved.
Fluctuations in the near steady-state will occur whenever short-term lead exposures are
superimposed on a long-term uptake pattern. Furthermore, the steady-state description is im-
perfect because on a very short (hourly) time scale, intake is not constant. Lead intake with
meals and changes in ambient air lead--outside to inside and vice versa—will cause quick
changes in exposure levels which may be viewed as short-term alterations in the small, labile
NEW10A/A 10-13 7/1/83
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PRELIMINARY DRAFT
lead pool. Metabolic stress could remobi1 ize and redistribute body stores, although documen-
tation of the extent to which this happens is very limited (Chisolm and Harrison, 1956).
10.3.1 lead in Blood
Viewed from different time scales, lead in whole blood may be seen as residing in several
distinct, interconnected pools. More than 99 percent of blood lead is associated with the
erythrocytes (DeSilva, 1981; Everson and Patterson, 1980; Manton and Cook, 1979) under typical
conditions, but it is the very small fraction of lead transported in plasma and extracellular
fluid that provides lead to the various body organs (Baloh, 1974).
Most of the erythrocyte lead is bound within the cell, although toxicity of the element
to the erythrocyte (Raghavan et al., 1981) is mainly associated with membrane lead content.
Within erythrocytes from non-exposed subjects, lead is primarily bound to hemoglobin, in par-
ticular HbA2, which binds approximately 50 percent of cell lead although it comprises only 1-2
percent of total hemoglobin (Bruenger et al., 1973). A further 5 percent is bound to a
10,000-dalton molecular weight fraction, about 20 percent to a much heavier molecule, and
about 25 percent is considered "free" or bound to lower weight molecules (Ong and Lee, 1980a;
Raghavan and Gonick, 1977). Raghavan et al. (1980) have observed that, among workers exposed
to lead, those who develop signs of toxicity at relatively low blood lead levels seem to have
a diminished binding of intracellular lead with the 10,000-dalton fraction, suggesting an im-
paired biosynthesis of a protective species. According to Ong and Lee (1980b), fetal hemo-
globin has a higher affinity for lead than adult hemoglobin. Whole blood lead in daily equi-
librium with other compartments was found to have a mean life of 35 days (25-day half-life)
and a total content of 1.9 mg, based on studies with a small number of subjects (Rabinowitz et
al., 1976). Chamberlain et al. (1978) established a similar, half-time for 203Pb in blood when
volunteers were given the label by ingestion, inhalation, or injection. The inhaled lead
studies in adults, described by Griffin et al. (1975), permit calculation of half-times of 28
and 26 days for inhalation of 10.4 and 3.1 pg Pb/m3 respectively.
Alterations in blood lead levels in response to abrupt changes in exposure apparently oc-
cur over somewhat different periods, depending on whether the direction of change is greater
or smaller. With increased lead intake, blood lead achieves a new value in approximately 60
days (Griffin et al., 1975; Tola et al., 1973), while a decrease may involve a longer period
of time, depending on the magnitude of the past higher exposure (0'Flaherty et al., 1982;
Rabinowitz et al. 1977; Gross, 1981). With age, there appears to be a modest increase in
blood lead, Awad et al. (1981) reporting an increase of 1 jig for each 14 years of age. In the
latter case, particularly with occupational exposure, it appears that the time for re-estab-
lishing near steady-state is more dependent upon the extent of lead resorption from bone and
the"total quantity deposited, extending the "washout" interval.
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PRELIMINARY DRAFT
Lead levels in newborn children are similar to but somewhat lower than those of their
mothers: 8.3 vs. 10.4 pg/dl (Buchet et al., 1978) and 11.0 vs. 12.4 pg/dl (Alexander and
Delves, 1981). Alexander and Delves (1981) also reported that maternal blood lead levels de-
crease throughout pregnancy, such decreases being greater than the expected dilution via the
concurrent increase in plasma volume. These data are consistent with increasing fetal uptake
during gestation (Barltrop, 1969). Increased tissue retention may also be a factor.
Levels of lead in blood are sex-related, adult women invariably showing lower levels than
adult males (e.g., Mahaffey et al., 1979). Of interest in this regard is the study of Stuik
(1974) showing lower blood lead response in women than in men for an equivalent level of lead
intake.
The small but biologically significant lead pool in blood plasma has proven technically
difficult to measure reliable values have become available only recently, and (see Chapter 9).
Chamberlain et al. (1978) found that injected 203Pb was removed from plasma (and, by infer-
ence, extracellular fluid) with a half-life of less than 1 hour. These data support the ob-
servation of DeSilva (1981) that lead is rapidly cleared from plasma. Ong and Lee (1980a), in
their in vitro studies, found that 203PB is virtually all bound to albumin and that only trace
amounts are bound to high weight globulins. It is not possible to state which binding form
constitutes an "active" fraction for movement to tissues.
Although Rosen et al. (1974) reported that plasma lead was invariant across a range of
whole blood levels, the findings of Everson and Patterson (1980), DeSilva (1981), and
Cavalleri et al. (1978) indicate that there is an equilibrium between red cell and plasma,
such that levels in plasma rise with levels in whole blood. This is consistent with the data
of Clarkson and Kench (1958) who found that lead in the red cell is relatively labile to ex-
change and a logical prerequisite for a dose-effect relationship in various organs. Ong and
Lee (1980c), furthermore, found that plasma calcium is capable of displacing RBC membrane
lead, suggesting that plasma calcium is a factor in the cell-plasma lead equilibrium.
10.3.2 Lead Levels in Tissues
Of necessity, various relationships of tissue lead to exposure and toxicity in humans
generally must be obtained from autopsy samples, although in some studies biopsy data have
been described. There is, then, the inherent question of how such samples adequately repre-
sent lead behavior in the living population, particularly in cases where death was preceded by
prolonged illness or disease states. Also, victims of fatal accidents are not well character-
ized as to exposure status, and are usually described as having no "known" lead exposures.
Finally, these studies are necessarily cross-sectional 1n design, and in the case of body
accumulation of lead it is assumed that different age groups have been similarly exposed.
Some Important aspects of the available data include the distribution of lead between soft and
NEW10A/A 10-15 7/1/83
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PRELIMINARY DRAFT
calcifying tissue, the effect of age and development on lead content of soft and mineral tis-
sue, and the relationship between total and "active" lead burdens in the body,
10.3.2.1 Soft Tissues. In humans after age 20 most soft tissues do not show age-related
changes in lead levels, in contrast to the case with bone (Barry and Mossman, 1970; Barry,
1975, 1981; Schroeder and Tipton, 1968; Butt et al., 1964). Kidney cortex also shows in-
creases in lead with age that may be associated with formation of lead nuclear inclusion
bodies (Indraprasit et al., 1974). Based on these rates of accumulation, the total body bur-
den may be divided into pools that behave differently: the largest and kinetically slowest
pool is the skeleton, which accumulates lead with age; and the much more labile lead pool is
in soft tissue.
Soft tissue levels generally stabilize in early adult life and show a turnover rate
similar to blood, sufficient to prevent accumulation except in the renal cortex, which may be
reflecting formation of lead-containing nuclear inclusion bodies (Cramer et al., 1974;
Indraprasit et al., 1974). The data of Gross et al. (1975) and Barry (1971) indicate that
aortic levels appear to rise with age, although this may reflect entrapment of lead in athero-
sclerotic deposits. Biliary and pancreatic secretions, while presumably reflecting some of
the organ levels, have tracer lead concentrations distinct from either blood or bone pools
(Rabinowitz et al., 1973).
For levels of lead in soft tissue, the reports of Barry (1975, 1981), Gross et al. (1975)
and Horiuchi et al. (1959) indicate that soft tissue lead content generally is below 0.5 jjg/g
wet weight, with higher values for aorta and kidney cortex. The higher values in aorta may or
may not reflect lead in plaque deposits, while higher kidney levels may be associated with the
presence of lead-accumulating tubular cell nuclear inclusions. The relatively constant lead
concentration in lung tissue across age groups suggests no accumulation of respired lead and
is consistent with data for deposition and absorption (see Section 10.2.2), Brain tissue was
generally under 0.2 ppm wet weight and appeared to show no change with increasing age. Since
these data were collected by cross-sectional study, age-related changes in the low levels of
lead in brain would have been difficult to discern. Barry (1975) found that tissues in a
small group of samples from subjects with known or suspected occupational exposure showed
higher lead levels in aorta, liver, brain, skin, pancreas, and prostate.
Levels of lead in whole brain are less illuminating to the issue of sensitivity of cer-
tain regions within the organ to toxic effects of lead than is regional analysis. The distri-
bution of lead across brain regions has been reported from various laboratories and the
relevant data for humans and animals are set forth in Table 10-2. The data of Grandjean
(1978) and Niklowitz and Mandybur (1975) for human adults, and those of Okazaki et al. (1963)
for autopsy samples from young children who died of lead poisoning, are consistent in showing
that lead is selectively accumulated in the hippocampus. The correlation of lead level with
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TABLE 10-2. REGIONAL DISTRIBUTION OF LEAD IN HUMANS ANO ANIMALS
Species
Exposure status
Relative distribution
Reference
Humans
Adult Males
Children
Adults
Animals
Adult rats
Adult rats
Unexposed
Fatal lead poisoning
Child, 2 yrs. old Fatal lead poisoning
3 subjects unexposed;
1 subject with lead
poisoning as child
Unexposed
Unexposed
Hippocampus s amygdala > medulla
oblongata > half brain > optic
tract s corpus callosum. Pb
correlated with K.
Hippocampus > frontal cortex »
occipital white matter, pons
Cortical gray matter > basal
gangli > cortical white matter
Hippocampus > cerebellum = temporal
lobes > frontal cortex in 3
unexposed subjects; temporal
lobes > frontal cortex >
hippocampus > cerebellum > in
case with prior exposure
Hippocampus > amygdala » whole
brain
Hippocampus had 50 percent of
brain lead with a 4:1 ratio
of hippocarapus:whole brain
Grandjean, 1978
Okazaki et al., 1963
Klein et al., 1970
Niklowitz and
Mandybur, 1975
Oanscher et al., 1975
Fjerdingstad et al.,
1974
-------
TABLE 10-2 (continued)
Species Exposure status Relative distribution Reference
Neonatal rats
Young dogs
Controls and
daily i.p. injection,
5.0 or 7.5 mg/kg
Controls and dietary
exposure, 100 ppm;
12 weeks of exposure
In both treated and control
animals: cerebellum > cerebral
cortex > brainstem + hippocampus
Klein and Koch, 1981
Controls: cerebellum = medulla >
caudate > occipital gray > frontal
gray
Exposed: occipital gray > frontal
gray = caudate > occipital
white = thalamus > medulla > cerebellum
Stowe et al., 1973
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PRELIMINARY DRAFT
potassium level suggests that uptake of lead is greater in cellulated areas. The involvement
of the cerebellum in lead encephalopathy in children (see Section 12.4) and in adult intoxica-
tion from occupational exposure indicates that the sensitivity of various brain regions to
lead as well as their relative uptake characteristics are factors in lead neuropathology.
In adult rats, selective uptake of .lead is shown by the hippocampus (Fjerdingstad et al.,
1974; Danscher et al., 1975) and the amygdala (Danscher et al., 1975). By contrast, lead-
exposed neonate rats show greatest uptake of lead into cerebellum, followed by cerebral cor-
tex, then brainstem plus hippocampus. Hence, there is a developmental difference in lead dis-
tribution in the rat with or without increased lead exposure (Klein and Koch, 1981).
In studies of young dogs, unexposed animals showed highest levels in the cerebellum,
while lead exposure was associated with selective uptake into gray matter; cerebellar levels
were relatively low. Unlike the young rat, then, the distribution of lead in brain regions of
dogs appears to be dose-dependent (Stowe et al., 1973).
Barry (1975, 1981) compared lead levels in soft tissues of children vs. adults. Tissue
lead of infants under 1 year old was generally lower than in older children, while children
aged 1-16 years had values that were comparable to adult women. In the Barry (1981) study,
the absolute concentration of lead in brain cortex or the ratios of brain cortex to blood lead
levels did not appear to be different in infants or older children compared to adults. Such
direct comparisons do not account for relative tissue mass changes with age, but this factor
is comparatively less with soft tissue than with the skeletal system (see Section 10.4).
Subcellular distribution of lead in soft tissue is not uniform, with high amounts of lead
being sequestered in the mitochondria and nucleus. Cramer et al. (1974) studied renal biops>
tissue in lead workers having exposures of variable duration and observed lead-binding nuclear
inclusion bodies in renal proximal tubules of subjects having short exposure, with all showing
mitochondrial changes. A considerable body of animal data (see Section 10.3.5) documents the
selective uptake of lead into these organelles. Pounds and Wright (1982) describe these
organellar pools in kinetic terms as having half-lives of comparatively short duration in cul-
tured rat hepatocytes, while McLachlin et al. (1980) found that rat kidney epithelial cells
form lead-sequestering nuclear inclusions within 24 hours.
10.3.2.2 Mineralizing Tissue. Biopsy and autopsy data have shown that lead becomes localized
and accumulates in human calcified tissues, i.e., bones and teeth. The accumulation begins
with fetal development (Barltrop, 1969; Horiuchi et al., 1959).
Total lead content in bone may exceed 200 mg in men aged 60 to 70 years, but in women the
accumulation is somewhat lower. Various investigators (Barry, 1975; Horiguchi and Utsonomiya,
1973; Schroeder and Tipton, 1968; Horiuchi et al., 1959) have documented that approximately 95
percent of total body lead is lodged in bone. These reports not only establish the affinity
of bone for lead, but also provide evidence that lead increases in bone until 50-60 years, the
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PRELIMINARY DRAFT
later fall-off reflecting some combination of diet and mineral metabolism changes. Tracer
data show accumulation in both trabecular and compact bone (Rabinowitz et al., 1976).
In adults, bone lead is the most inert pool as well as the largest, and accumulation can
serve to maintain elevated blood lead levels years after past, particularly occupational, ex-
posure has ended. This accounts for the observation that duration of exposure correlates with
the rate of reduction of blood lead after termination of exposure (O'Flaherty et al., 1982).
The proportion of body lead lodged in bone is reported to be lower in children than in adults,
although concentrations of lead in bone increase more rapidly than in soft tissue during
childhood (Barry, 1975, 1981). In 23 children, bone lead was 9 mg, or 73 percent of total
body burden vs. 94 percent in adults. Expression of lead in bone in terms of concentration
across age groups, however, does not accommodate the "dilution" factor, which is quite large
for the skeletal system in children (see Section 10.4).
The isotope kinetic data of Rabinowitz et al. (1976) and Holtzman (1978) indicate biolo-
gical half-times of lead in bone on the order of several decades, although it appears that
there are two bone compartments, one of which is a repository for relatively labile lead
(Rabinowitz et al., 1977).
Tooth lead levels also increase with age at a rate proportional to exposure (Steenhout
and Pourtois, 1981), and are also roughly proportional to blood lead levels in man (Winneke et
al., 1981) and experimental animals (Kaplan et al., 1980). Dentine lead is perhaps the most
responsive component of teeth to lead exposure since it is laid down from the time of eruption
until the tooth is shed. Needleman and Shapiro (1974) have documented the utility of dentine
lead as an indicator of the degree of subject exposure. Fremlin and Edmonds (1980), using
alpha particle excitation and micro-autoradiography, have shown dentine zones of lead enrich-
ment related to abrupt changes in exposure. The rate of lead deposition in teeth appears to
vary with the type of tooth, being highest in the central incisors and lowest in the molars, a
difference that must be taken into account when using tooth lead data for exposure assessment,
particularly for low levels of lead exposure (Mackie et al., 1977; Delves et al., 1982).
10.3.3 Chelatable lead
Mobile lead in organs and systems is potentially more "active" toxicologically in terms
of being available to sites of action. Hence, the presence of diffusible, mobilizable, or ex-
changeable lead may be a more significant predictor of imminent toxicity or recent exposure
than total body or whole blood burdens. In reality, however, these would be quite difficult
assays.
In this regard, "chelatable" urinary lead has been shown to provide an index of this
mobile portion of total body burden. Chelation challenge is now viewed as the most useful
probe of undue body burden in children and adults (U.S. Centers for Disease Control, 1978;
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PRELIMINARY DRAFT
World Health Organization, 1977; Chisolm and Barltrop, 1979; Chisolm et al., 1976; Saenger et
al., 1982; Hansen et al., 1981), based mainly on the relationship of chelatable lead to in-
dices of heme biosynthesis impairment. In general, the amount of plumburesis associated with
chelant challenge is related to the dose and the schedule of administration.
A quantitative description of Inputs to the fraction of body lead that is chelatable from
various body compartments is difficult to fully define, but it very likely includes a sizable,
fairly mobile compartment within bone as well as soft tissues this assertion is based on: 1)
the fact that the amount of lead mobilized by chelation is age dependent in non-exposed adults
(Araki, 1973; Araki and Ushio, 1982) while blood and soft tissue lead levels are not (Barry,
1975), indicating a lead pool labile to chelation but kinetically distinct from soft tissue;
2) the studies of chelatable lead in animals (Hammond, 1971, 1973) suggesting removal of some
bone lead fraction and the response of explanted fetal rat bone lead to chelants (Rosen and
Markowitz, 1980); 3) the tracer modeling estimates of Rabinowitz et al. (1977) which suggest a
mobile bone compartment; and 4) the complex, non-linear relationship of lead intake by air,
food, and water (see Chapter 11) to blood lead, as well as the exponential relationship of
chelatable lead to blood lead (Chisolm et al., 1976).
The logarithmic relationship of chelatable lead to blood lead in children (Chisolm et
al., 1976) is consistent with the studies of Saenger et al. (1982), who reported that levels
of mobilizable lead in "asymptomatic" children with moderate elevations in blood lead were
quite similar in many cases to those values obtained in children with signs of overt toxicity.
Hansen et al. (1981) reported that lead workers challenged with CaNa2EDTA showed 24-hour urine
lead levels that in many cases exceeded the accepted limit levels even though blood lead was
only moderately elevated in many of those workers. The action level corresponded, on the re-
gression curve, to a blood value of 35 Mfl/dl.
Several reports provide insight into the behavior of labile lead pools in children
treated with chelating agents over varying periods of time. Treatment regimens using
CaNa2EDTA or CaNa2EDTA + BAL for up to 5 days have been Invariably associated with "rebound"
in blood lead, ascribed to a redistribution of lead among mobile lead compartments (Chisolm
and Barltrop, 1979). Marcus (1982) reported that 41 children given oral D-penicillamine for 3
months showed a significant drop in blood lead by 2 weeks (mean initial value of 53,2 Hfl/dl)
then a slight rise that was within measurement error with a peak at 4 weeks, and a fall at 6
weeks, followed by no further change at a blood lead of 36 |ig/dl. Hence, there was a near
steady-state at an elevated level for 10 of the 12 weeks with continued treatment. This ob-
servation may indicate that re-exposure was occurring, with oral penicillamine and ingested
lead leading to increased lead uptake, as seen by Jugo et al. (1975a). However, Marcus
states that an effort was made to limit further lead intake as much as possible. From these
reports. It appears that a re-equilibration does occur, varying in characteristics with type
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PRELIMINARY DRAFT
and duration of chelation. The rebound seen in short-term treatment with CaNa2E0TA or
CaNa2EDTA + BAL, although »itributed to soft tissue, could well include a shift of lead from a
larger mobile bone compartment to soft tissues and blood. The apparent steady state between
the blood lead pool and other compartments that is achieved in the face of plumburesis, in-
duced by D-penicillamine (Marcus, 1982), suggests a rather sizable labile body pool which, in
quantitative terms, would appear to exceed that of soft tissue alone,
10.3.4 Mathematical Descriptions of Physiological Lead Kinetics
In order to account for observed kinetic data and make predictive statements, a variety
of mathematical models have been suggested, including those describing "steady state" condi-
tions. Tracer experiments have suggested conpartmental models of lead turnover based on a
central blood pool (Holtzman, 1978; Rabinowitz et al., 1976; Batschelet et al., 1979). These
experiments have hypothesized well-mixed, Interconnected pools and have utilized coupled dif-
ferential equations with linear exponential solutions to predict blood and tissue lead ex-
change rates. Were lead to be retained in these pools in accordance with a power-law distri-
bution of residence times, rather than being uniform, a semi-Markov model would be more appro-
priate (Marcus, 1979).
Lead pools with more rapid turnover than whole blood (on the order of minutes) have been
detected within isolated cells (Pounds and Wright, 1982). Evidence of an extracellular lead
pool in humans exists in observations of lead plasma (DeSilva, 1981) and urine (Rabinowitz et
al., 1974) after oral lead exposure, as well as from 203Pb studies using injection, ingestion,
and inhalation exposure routes (Chamberlain and Heard, 1981). No single model has been deve-
loped to utilize what has been learned about lead behavior in these highly labile pools
existing around and within permanent and concentrated sites.
Extant steady-state models are also deficient, not only because they are based on small
numbers of subjects but also because there may be a dose dependency for some of the interpool
transfer coefficients. In this case, a non-linear dose-indicator response model would be more
appropriate when considering changes 1n blood lead levels. For example, the relationship
between blood lead and air lead (Hammond et al., 1981) as well as that for diet (United
Kingdom Central Directorate on Environmental Pollution, 1982) and tap drinking water (Sherlock
et al., 1982) are all non-linear in mathematical form. In addition, alterations in
nutritional status or the onset of metabolic stresses can complicate steady-state relation-
ships.
The above discussions of both the non-linear relationship of intake to the blood lead
pool and the non-linear relationship of chelatable, or toxicologically active, lead to blood
levels logically indicate that intake at elevated levels can add substantially to this
chelatable pool and be substantially unrecognized in blood lead measurements.
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PRELIMINARY DRAFT
10.3.5 Animal Studies
The relevant questions to be asked of animal data are those that cannot be readily or
fully satisfied in human subjects: (1) What is the effect of exposure level on distribution
within the body at specific time points? (2) What 1s the relationship of age or developmental
stage on the distribution of lead in organs and systems, particularly the nervous system?
(3) What are the relationships of physiological stress and nutritional status to the redistri-
bution kinetics? (4) Can the relationship of chelatable lead to such indicator lead pools as
blood be defined better?
Administration of a single dose of lead to rats produces high initial lead concentrations
in soft tissues, which then fall rapidly as the result of excretion and transfer to bone
(Hammond, 1971), while the distribution of lead appears to be Independent of the dose.
Castellino and A1oj (1964) reported that single dose exposure of rats to lead was associated
with a fairly constant ratio of red cell to plasma, a rapid distribution to tissues and rela-
tively higher uptake in liver, kidney, and particularly bone. Lead loss from organs and tis-
sues follow first-order kinetics except for bone. The data of Morgan et al. (1977),
Castellino and Aloj (1964), and Keller and Doherty (1980a) document that the skeletal system
in rats and mice is the kinetically rate-limiting step in whole-body lead clearance.
Subcellular distribution studies involving either tissue fractionation after i_n vivo lead
exposure or jn vitro data document that lead is preferentially sequestered in the nucleus
(Castellino and Aloj, 1964; Goyer et al., 1970) and mitochondrial fractions (Castellino and
Aloj, 1964; Barltrop et al., 1974) of cells from lead-exposed animals. Lead enrichment in the
mitochondrion is consistent with the high sensitivity of this organelle to the toxic effects
of lead.
The neonatal animal seems to retain proportionately higher levels of tissue lead compared
with the adult (Goldstein et al., 1974; Momcilovid and Kostial, 1974; MykkSnen et al., 1979;
Klein and Koch, 1981) and shows slow decay of brain lead levels while other tissue levels sig-
nificantly decrease over time. This appears to be the result of enhanced entry by lead due to
a poorly developed brain barrier system in the developing animals, as well as enhanced body
retention in the young animals. The effects of such changes as metabolic stress and nutri-
tional status have been noted in the literature, Keller and Ooherty (1980b) have documented
that tissue redistribution of lead, specifically bone lead mobilization, occurs in lactating
female mice, both lead and calcium transfer occurring from mother to pups. Changes in lead
movement from body compartments, particularly bone, with changes in nutrition are described In
Section 10.5.
In studies with rats that are relevant both to the issue of chelatable lead vs. lead in-
dicators in humans and to the relative lability of lead in the young vs. the adult, Jugo et
al. (1975b) and Jugo (1980) studied the chelatability of lead in neonate vs. adult rats and
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PRELIMINARY DRAFT
Its lability in the erythrocyte. Challenging young rats with metal che1ants yielded propor-
tionately lower levels of urinary lead than in the adult, a finding that has been ascribed to
tighter binding of lead in the young animal (Jugo et al., 1975b). In a related observation,
the chelatable fraction of lead bound to erythrocytes of young animals given soapij was approx-
imately 3-fold greater than in the adult rat (Jugo, 1980), although the fraction of dose in
the cells was higher in the suckling rat. The difference in the suckling rat erythrocyte re-
garding the binding of lead and relative content compared with the adult may be compared with
the Ong and lee's (1980b) observation that human fetal hemoglobin binds lead more avidly than
does mature hemoglobin.
10.4 LEAD EXCRETION AND RETENTION IN HUMANS AND ANIMALS
Dietary lead in humans and animals that is not absorbed passes through the gastro-
intestinal tract and is eliminated with feces, as Is that deposited fraction of air lead that
is swallowed and not absorbed. Lead absorbed into the blood stream and not retained is excre-
ted through the renal and gastrointestinal tracts, the latter by biliary clearance. The
amounts appearing in urine and feces appear to be a function of such factors as species, age,
and differences in dosing.
10.4.1 Human Studies
Booker et al. (1969) found that 212Pb injected into two adult volunteers led to initial
appearance of the label first in urine (4.4 percent of dose in 24 hours), then in both urine
and feces in approximately equal amounts. By use of the stable isotope 204Pb, Rabinowitz et
al. (1973) reported that urinary and fecal excretion of the label amounted to 38 and 8 yg/day
1n adult subjects, accounting for 76 and 16 percent, respectively, of the measured recovery.
Fecal excretion was thus approximately twice that of all the remaining modes of excretion:
hair, sweat, and nails (8 percent).
Perhaps the most detailed study of lead excretion in adult humans was done by Chamberlain
et al. (1978), who used 203Pb administered by injection, inhalation and ingestion. Following
injection or oral Intake, the amounts in urine (Pb-U) and feces (Pb-Fe, endogenous fecal lead)
were compared for the two administration routes. Endogenous fecal lead was 50 percent of that
in urine, or a 2:1 ratio of urinary/fecal lead, after allowing for increased transit time of
fecal lead through the 61 tract.
Based on the metabolic balance and isotope excretion data of Kehoe (1961a,b,c),
Rabinowitz et al. (1976), and Chamberlain et al. (1978), as well as some recalculations of the
Kehoe and Rabinowitz data by Chamberlain et al. (1978), it appears that short-term lead excre-
tion amounts to 50-60 percent of the absorbed fraction, the balance moving primarily to bone
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PRELIMINARY DRAFT
TABLE 10-3. COMPARATIVE EXCRETION AND RETENTION
RATES IN ADULTS AND INFANTS
Children*5
Adult
group A
Adult
group B1
Dietary Intake (jig/kfl)
10.76
3.63
3.86
Fraction absorbed®
0.46 (0.55)f
0.15®
0.15®
Diet lead absorbed (^ig/kg)
4.95 (5.92)
0.54
0.58
Air lead absorbed (Hg/kg)
0.20
0.21
0.11
Total absorbed lead (jig/kg
5.15 (6,12)
0.75
0.68
Daily urinary Pb (pg/kg)
1.00
0.47
0.34
Ratio: urinary/absorbed Pb
0.19 (0.16)
0.62
0.24*
0.50
0.171
Endogenous fecal Pb
0.5 (1.56)h
Total excreted Pb
1.50 (2.56)
0.71
0.51
Ratio: total excreted/
absorbed Pb
0.29 (0.42)
0.92
0.75
Fraction of intake retained
0.34 (0.33)
0.01
0.04
jWkg-day.
Ziegler et al., 1978.
^Rabinowitz et al., 1977.
Thompson, 1971, and estimates of Chamberlain et al., 1978.
^Corrected for endogenous fecal Pb; Pb-Fe - 0,5 x Pb-U.
Corrected for endogenous fecal Pb at extrapolated value from
Ziegler et al., 1978.
"Corrected for Pb-Fe.
.Extrapolated value for endogenous fecal Pb of 1.56.
For a ratio of 0.5, Pb-Fe/Pb-U.
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with some subsequent fraction, (approximately half) of this stored amount eventually being
excreted. The rapidly excreted fraction was determined by Chamberlain et al. (1978) to have
an excretion half-time of about 19 days. This Is consistent with the estimates of Rabinowitz
et al. (1976), who expressed clearance in terms of mean-times. Mean-times are multiplied by
In 2 (0.693) to arrive at half-times. The similarity of blood 203Pb half-times with that of
body excretion noted by Chamberlain et al. (1978) indicates a steady rate of clearance from
the body.
The age dependency of lead excretion rates in humans, has not been well studied, for all
of the above lead excretion data involved only adults. Table 10-3 combines available data
from adults and infants for purposes of comparison. Intake, urine, fecal, and endogenous
fecal lead data from two studies involving adults and one. report with infants are used. For
consistency in the adult data, 70 kg is used as an average adult weight, and a Pb-Fe/Pb-U
value of 0.5 used. Lead Intake, absorption, and excretion are expressed as pg Pb/kg/day. For
the Zlegler et al. (1978) data with infants, endogenous fecal lead excretion is calculated
using the adult ratio as well as the extrapolated value of 1.5 pg Pb/kg/day. The respiratory
intake value for the infants is an upper value (0.2 pg Pb/m8), since Ziegler et al. found air
lead to be <0.2 pg/m3. In comparison with the two representative adult groups, infants appear
to have a lower total excretion rate, although the excretion of endogenous fecal lead may be
higher than for adults.
Lead is accumulated in the human body with age, mainly in bone, up to approximately 60
years of age, when a decrease occurs with changes in intake as well as in bone mineral
metabolism. Total accumulation by 60 years of age ranges up to approximately 200 mg (see
review by Barry, 1978), although occupational exposure can raise this figure several-fold
(Barry, 1975). Holtzman (1978) has reviewed the available literature on studies of lead
retention In bone. In normally exposed humans a biological half-time of approximately 17
years has been calculated, while data for uranium miners yield a range of 1320-7000 days (4-19
years). Chamberlain et al. (1978) have estimated life-time averaged daily retention at 9.5 pg
using data of Barry (1975). Within shorter time frames, however, retention can vary con-
siderably due to such factors as disruption of the individual's equilibrium with lead intake
at a given level of exposure, the differences between children and adults, and, in elderly
subjects, the presence of osteoporosis (Gross and Pfitzer, 1974).
Lead labeling experiments, such as those of Chamberlain et al. (1978), indicate a short-
term or initial retention of approximately 40-50 percent of the fraction absorbed, much of
which is by bone. It is difficult to determine how much lead resorption from bone will even-
tually occur using labeled lead, given the extremely small fraction of labeled to unlabeled
lead (i.e., label dilution) that would exist. Based on the estimates of Kehoe (1961a,b,c),
the Gross (1981) evaluation of the Kehoe studies, the Rabinowitz et al. (1976) study, the
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PRELIMINARY DRAFT
Chamberlain et al. (1978) assessments of the aforementioned reports, and the data of Thompson
(1971), approximately 25 percent of the lead absorbed daily undergoes long-term bone storage.
The above estimates relate either to adults or to long-term retention over most of an
individual's lifetime. Studies with children and developing animals (see Section 10.4.2)
indicate lead retention in childhood can be higher than in adults. By means of metabolic
balance studies, Ziegler et al. (1978) obtained a retention figure (as percentage of total
intake) of 31.5 percent for infants, while of Alexander et al. (1973) provided an estimate of
18 percent. Corrected retention data for both total and absorbed intake for the pediatric
subjects of Ziegler et al. (1978) are shown in Table 10.3, using the two values for endogenous
fecal excretion as noted. Barltrop and Strehlow (1978) calculated a net negative lead reten-
tion in their subjects, but problems in comparing this report with the others were noted
above. Given the increased retention of lead 1n children relative to adults, as well as the
greater rate of lead intake on a body weight basis, increased uptake in soft tissues and/or
bone 1s indicated. \
Barry (1975, 1981) measured the lead content of soft and mineral tissue in a small group
of autopsy samples from children 16 years of age and under, and noted that average soft tissue
values were comparable to those in female adults, while mean bone lead values were lower than
in adults. This suggests that bone 1n children has less retention capacity for lead than
adults. It should be noted, however, that "dilution" of bone lead will occur because of the
significant growth rate of the skeletal system through childhood. Trotter and Hixon (1974)
studied changes in skeletal mass, density, and mineral content as a function of age, and noted
that skeletal mass Increases exponentially in children until the early teens, increases less
up to the early 20s, levels off in adulthood, and then slowly decreases. From infancy to the
late teens, bone mass Increases up to 40-fold. Barry (1975) noted an approximate doubling in
bone lead concentration over this interval, indicating that total skeletal lead had actually
increased 80-fold, and obtained a mean total bone lead content up to 16 years of approximately
8 mg, compared with a value of approximately 18 mg estimated from both the bone concentrations
in his study at different ages and the bone growth data of Trotter and Hixon (1974). In a
later study (Barry, 1981), autopsy samples from infants and children between 1 and 9 years old
showed an approximate 3.5-fold increase in mean bone concentrations across the three bone
types studied, compared with a skeletal mass increase from 0-6 mos. to 3-13 years old of
greater than 10-fold, for an estimated increase in total lead of approximately 35-fold. Five
reports (see Barry, 1981) noted age vs. tissue lead relationships indicating that overall bone
lead levels in infants and children were less than in adults, whereas while 4 reports observed
comparable levels in children and adults.
If one estimates total daily retention of lead in the infants studied by Ziegler et al.
(1978), using a mean body weight of approximately 10 kg and the corrected retention rate 1n
Table 10.3, one obtains a total daily retention of approximately 40 pg Pb. By contrast, the
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PRELIMINARY DRAFT
total reported or estimated skeletal lead accumulated between 2 and 14 years 1s 8-18 mg (vide
supra), which averages out to a dally long-term retention of 2.0-4.5 pg/day or 6-13 percent of
total retention. It may be the case that lead retention is highest in infants up to about 2
years of age (the subjects of the Zlegler et al. study), then decreases in older children.
The mean retention in the Alexander et al. (1973) study wis 18 percent, about half that seen
by Zlegler et al. (1978). This difference is possibly due to the greater age range in the
former study.
"Normal" blood lead levels in children either parallel adult males or are approximately
30 percent greater than adult females (Chamberlain et al., 1978), indicating (1) that the soft
tissue lead pool in very young children is not greatly elevated and thus, (2) that there is a
huge labile lead pool in bone which is still kinetically quite distinct from soft tissue lead
or (3) that in young children, blood lead 1s a much less reliable Indicator of greatly ele-
vated soft tissue or labile bone lead than 1s the case with adults. Barry (1981) found that
soft tissue lead levels were comparable in infants SI year old and children 1-5 and 6-9 years
old.
Given the Implications of the above discussion, that retention of lead in the young child
is higher than in adults and possibly older children, while at the same time their skeletal
system 1s less effective for long-term lead sequestration, the very young child 1s at greatly
elevated risk to a toxicologically "active" lead burden. For a more detailed discussion, see
Chapter 13.
10.4.2 Animal Studies
In rats and other experimental animals, both urinary and fecal excretion appear to be
important routes of lead removal from the organism; the relative partitioning between the two
modes 1s species and dose dependent. Morgan et al. (1977), injected !03Pb Into adult rats and
noted that lead initially appeared in urine, followed by equivalent elimination by both
routes; by 5 days, lead was proportionately higher in feces. CastelUno and Aloj (1964),
using 210Pb, observed that fecal excretion was approximately twice that of urine (35.7 vs.
15.9 percent) by 14 days. In the report of Klaassen and Shoeman (1974), relative excretion by
the two routes was seen to be dose-dependent up to 1.0 mg/kg, being much higher by biliary
clearance into the gut. At 3.0 mg/kg, approximately 90 percent of the excreted amount was
detected in feces. The relatively higher proportion appearing in feces in the studies of
CastelUno and Aloj (1964) and Klaassen and Shoeman (1974), compared with the results of
Morgan et al. (1977), is possibly due to the use of carrier dosing, since Morgan et al. (1977)
used carrier-free Injections. Hence, it appears that increasing dose does favor biliary excre-
tion, as noted by Klaassen and Shoeman (1974).
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PRELIMINARY DRAFT
With regard to species differences, Klaassen and Shoeman (1974) found that the amount of
biliary clearance in dogs was about 2 percent of that in rats, while rabbits showed 50 percent
of the rate of the rat at equivalent dosing. These data for the dog are in contrast to the
results of Lloyd et al. (1975), who observed 75 percent of the excreted lead eliminated
through biliary clearance. It should be noted that the latter researchers used carrier-free
label while the other investigators used injections with carrier at 3.0 mg Pb/kg levels. In
mice, Keller and Doherty (1980a) observed that the cumulative excretion rate of 210 Pb in urine
was 25-50 percent of that in feces. In nonhuman primates, Cohen (1970) observed that baboons
excreted lead at the rate of 40 percent in feces and 60 percent in urine. Pounds et al.
(1978) noted that the Rhesus monkey lost 30 percent of lead by renal excretion and 70 percent
in feces. This may also be reflecting a carrier dosing difference.
The extent of total lead excretion in experimental animals given labeled lead orally or
parenterally varies, in part due to the time frames for post-exposure observation. In the
adult rat, Morgan et al. (1977) found that 62 percent of injected 203Pb was excreted by €
days. By 8 days, 66 percent of injected 203Pb was eliminated in the adult rats studied by
Momcilovitf and Kostial (1974), while the 210Pb excretion data of Castellino and Aloj (1964)
for the adult rat showed 52 percent excreted by 14 days. Similar data were obtained by
Klaassen and Shoeman (1974). Lloyd et al. (1975) found that dogs excreted 52 percent of
injected lead label by 21 days, 83 percent by 1 year, and 87 percent by 2 years. In adult
mice (Keller and Ooherty, 1980a), 62 percent of injected lead label was eliminated by 50 days.
In the nonhuman primate, Pounds et al. (1978) measured approximately 18 percent excretion in
adult Rhesus monkeys by 4 days.
Kinetic studies of lead elimination in experimental animals indicate that excretion is
described by two or more components. From the elimination data of Momeilovid and Kostial
(1974), Morgan et al. (1977) estimated that in the rat the excretion curve obeys a two-compo-
nent exponential expression with half-times of 21 and 280 hours. In dogs, Lloyd et al. (1975)
found that excretion could be described by three components, i.e., a sum of exponentials with
half-times of 12 days, 184 days, and 4951 days. Keller and Doherty (1980a) reported that the
half-time of whole-body clearance of injected 203Pb consisted of an initial rapid and a much
slower terminal component, the latter having a half-time of 110 days in the adult mouse.
The excretion rate dependency on dose level has been investigated in several studies.
Although Castellino and Aloj (1964) saw no difference in total excretion rate when label was
injected with 7 or 100 '^9 of carrier, Klaassen and Shoeman (1974) did observe that the excre-
tion rate by biliary tract was dose dependent at 0.1, 1.0, and 3.0 mg Pb/kg (urine values were
not provided for obtaining estimates of total excretion). Momeilovid and Kostial (1974) saw
increased rate of excretion into urine over the added carrier range of 0.1 to 2.0 pg Pb with
no change in fecal excretion. In the report of Aungst et al. (1981) there was no change in
NEW10A/A 10-29 7/1/83
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PRELIMINARY DRAFT
excretion rate in the rat over the injected lead dosing range of 1,0 to 15.0 mg/kg. It thus
appears that rat urinary excretion rates are dose-dependent over a narrow range less than <7
pg, while elimination of lead through biliary clearance is dose-dependent up to an exposure
level of 3 mg Pb/kg.
Lead movement from lactating animals to their offspring via milk constitutes both a route
of excretion for the mother and a route of exposure to lead for the young. Investigations
directed at this phenomenon have examined both prior-plus-ongoing maternal lead exposure
during lactation and the effects of immediate prior treatment. Keller and Doherty (1980b)
exposed two groups of female rats to 210Pb-labeled lead: one group for 105 days before mat-
ing; the second before and during gestation and nursing. During lactation, there was an over-
all loss of lead from the bodies of the lactating females compared with controls while the
femur ash weights were inversely related to level of lead excretion, indicating that such
enhancement is related to bone mineral metabolism. Lead transfer via milk was approximately
3 percent of maternal body burden, increasing with continued lead exposure during lactation.
Lorenzo et al. (1977) found that blood lead in nursing rabbits given injected lead peaks
rather rapidly (within 1 hour), while milk lead shows a continuous increase for about 8 days,
at which point its concentration of lead is 8-fold higher than blood. This indicates that
lead transfer to milk can occur against a concentration gradient in blood. Motncilovic (1978)
and Kostial and Moracilovid (1974) observed that transfer of 203Pb in the late stage of lacta-
tion occurs readily in the rat, with higher overall excretion of lead in nursing vs. control
females. Furthermore, it appeared that the rate of lead movement to milk was dose-dependent
over the added lead carrier range of 0.2-2.0 pg Pb.
The comparative retention of lead in developing vs. adult animals has been investigated
in several studies using rats, mice, and nonhuman primates. Momcilovic and Kostial (1974)
compared the kinetics of lead distribution in suckling vs. adult rats after injection of
203Pb. Over an 8-day interval, 85 percent of the label was retained in the suckling rat,
compared with 34 percent in the adult. Keller and Doherty (1980a) compared the levels of
2i0Pb in 10-day-old mice and adults, noting from the clearance half-times (vide supra) that
lead retention was greater in the suckling animals than in the adults. In both adult and
young mice, the rate of long-term retention was governed by the rate of release of lead from
bone, indicating that in the mouse, skeletal lead retention in the young is greater than in
the adult. With infant and adult monkeys orally exposed-to 210Pb, Pounds et al. (1978)
observed that at 23 days the corresponding amounts of initial dose retained were 92.7 and 81.7
percent, respectively.
The studies of Rader et al. (1981; 1982) are of particular interest as they not only
demonstrate that young experimental animals continue to show greater retention of lead in
tissue when exposure occurs after weaning, but also that such retention occurs in terms of
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PRELIMINARY DRAFT
either uniform exposure (Rader et al., 1981) or uniform dosing (Rader et al,, 1982) when com-
pared with adult animals. With uniform exposure, 30-day-old rats given lead in drinking water
showed significantly higher lead levels in blood and higher percentages of dose retained in
brain, femur, and kidney, as well as higher indices (ALA-U, EP) of hematopoietic impairment
when compared with adult animals. As a percentage of dose retained, tissues in the young ani-
mals were approximately 2-3-fold higher. In part, the difference is due to a higher ingestion
rate of lead. However, in the uniform dosing study where this was not the case, an increased
retention of lead still prevailed, the amount of lead in brain being approximately 50 percent
higher in young vs. adult animals. Comparison of values in terms of percent retained is more
meaningful for such assessments, because the factor of changes in organ mass (see above) is
taken into account. Delayed excretion in the young animal may reflect an immature excretory
system or a tighter binding of lead in various body compartments.
10.5 INTERACTIONS OF LEAD WITH ESSENTIAL METALS AND OTHER FACTORS
Deleterious agents, particularly toxic metals such as lead, do not express their toxico-
kinetic or toxicological behavior in a physiological vacuum, but rather are affected by inter-
actions of the agent with a variety of biochemical factors such as nutrients. Growing recog-
nition of this phenomenon and its implications for lead toxicity in humans have prompted a
number of studies, many of them recent, that address both the scope and mechanistic nature of
such interactive behavior.
10.5.1 Human Studies
In humans, the interactive behavior of lead and various nutritional factors is appropri-
ately viewed as being particularly significant for children, since this age group is not only
particularly sensitive to lead's effects, but also represents the time of greatest flux in
relative nutrient status. Such interactions occur against a backdrop of rather widespread
deficiencies in a number of nutritional components in children. While such deficiencies are
more pronounced in lower income groups, they exist in all socioeconomic strata. Mahaffey and
Michael son (1980) have summarized the three nutritional status surveys carried out in the
United States for infants and young children: the Preschool Nutrition Survey, the Ten State
Nutrition Survey, and the National Health Assessment and Nutritional Evaluation Survey (NHANES
I). The most recent body of data of this type is the NHANES II study (Mahaffey et al., 1979),
although the dietary information from it has yet is to be reported. In the older surveys,
iron deficiency was the most common nutritional deficit in children under 2 years of age,
particularly children from low-income groups. Reduced vitamin C Intake was noted in about
one-third of the children, while sizable numbers of them had significantly reduced intakes of
NEW10A/A 10-31 7/1/83
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PRELIMINARY DRAFT
calcium. Owen and Lippmann (1977) reviewed the regional surveys of low-income groups within
Hispanic, white, and black populations. In these groups, Iron deficiency was a common
finding, while low intakes of calcium and vitamins A and C were observed regularly. Hambidge
(1977) concluded that zinc intake in low-income groups is generally inadequate, relative to
recommended daily allowances.
Available data from a number of reports document the association of lead absorption with
suboptimal nutritional status. Mahaffey et al. (1976) summarized their studies showing that
children with blood lead greater than 40 (jg/dl had significantly (p <0.01) lower intake of
phosphorus and calcium compared with a control group, while Iron intake in the two groups was
comparable. This study Involved children 1-4 years old from an 1nner-c1ty, low-income popula-
tion, with close matching for all parameters ^except the blood lead level. Sorrel 1 et al.
(1977), in their nutritional assessment of 1- to 4-year-old children with a range of blood
lead levels, observed that blood lead content was inversely correlated with calcium intake,
while children with blood lead levels >60 pg/dl had significantly (p <0.001) lower intakes of
calcium and vitamin D.
Rosen et al. (1981) found that children with elevated blood lead (33-120 pg/dl) had sig-
nificantly lower serum concentrations of the vitamin D metabolite 1,25-(0H)2D (p <0.001) com-
pared with age-matched controls, and showed a negative correlation of serum 1,25-(0H)2D with
lead over the range of blood leads measured. These observations and animal data (Barton et
al., 1978a, see Section 10.5.2) may suggest an increasingly adverse interactive cycle of
1,25-(0H)2D, lead, and calcium in which lead reduces biosynthesis of the vitamin D metabolite.
This then leads to reduced induction of calcium binding protein (CaBP), less absorption of
calcium from the gut, and greater uptake of lead, thus increasing uptake of lead and further
reducing metabolite levels. Barton et al. (1978a) isolated two mucosal proteins in rat intes-
tine, one of which bound mainly lead and was not vitamin D-stimulated; the second bound mainly
calcium and was under vitamin control. The authors suggested direct site binding competition
between lead and calcium in these proteins. Hunter (1978) investigated the possible inter-
active role of seasonal vitamin D biosynthesis in adults and children; it 1s a common obser-
vation that lead poisoning occurs more often in summer than in other seasons (see Hunter,
1977, for review). In children, seasonality accounts for 16 percent of explained variance
of blood lead in black children, 12 percent in Hispanics, and 4 percent in whites. More
recently, it has been documented that there is no seasonal variation in circulating levels of
1,25-(0H)2D the metabolite that affects the rate of lead absorption from the GI tract (Chesney
et al., 1981). These results suggest that seasonality is related to changes in exposure.
Johnson and Tenuta (1979) determined that calcium intake was negatively correlated
(r = -0.327, p <0.05) with blood lead in 43 children aged 1-6 years. The high lead group also
consumed less zinc than children with lower blood levels. Yip et al. (1981) found that 43
NEW10A/A 10-32 7/1/83
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PRELIMINARY DRAFT
children with elevated blood lead (>30 pg/dl) and EP (>35 pg/dl) had an Increased prevalence
of iron deficiency as these two parameters increased. Children classed as CDC lb and II had a
79 percent deficiency rate, while those in Class III were all iron-deficient. Chisolm (1981)
demonstrated an inverse relationship between "chelatable" iron and chelatable body lead levels
as indexed by urinary ALA levels in 66 children with elevated blood lead. Watson et al.
(1980) reported that adult subjects who were iron-deficient (determined from serum ferritin
measurement) showed a lead absorption rate 2-3 times greater than subjects who were iron
replete. In a group of 13 children, Markowitz and Rosen (1981) reported that the mean serum
zinc levels in qhildren with plumbism were significantly below the values seen in normal chil-
dren. Chelation therapy reduced the mean level even further. Chisolm (1981) reported that
there was an inverse relationship between ALA-U and the amount of "chelatable" or systemlcally
active zinc in 66 children challenged with EDTA and having blood lead levels ranging from 45
to 60 pg Pb/dl. These two studies suggest that zinc status is probably as important an inter-
active modifier of lead toxicity as is either calcium or iron.
The role of nutrients in lead absorption has been reported in several metabolic balance
studies for both adults and children. Ziegler et al. (1978), in their investigations of lead
absorption and retention in infants, observed that lead retention was inversely correlated
with calcium intake, expressed either as intake percentage (r = -0.284, ,p <0.01) or on a
weight basis (r = -0.279, p <0.01). Of interest 1s the fact that the range of calcium intake
measured was within the range considered adequate for infants and toddlers by the National
Research Council (National Academy of Sciences, National Research Council, 1974). These data
also support the premise that severe deficiency need not be present for an interactive rela-
tionship to occur. Using adults, Heard and Chamberlain (1982) monitored the uptake of 203Pb
from the gut in eight subjects as a function of the amounts of dietary calcium and phosphorus.
Without supplementation with either of these minerals 1n fasting subjects, the label absorp-
tion rate was approximately 60 percent, compared with 10 percent with 200 mg calcium plus
140 mg phosphorus, the amounts present in an average meal. Calcium alone reduced uptake by a
factor of 1.3 and phosphorus alone by 1.2; both together yielded a reduction factor of 6.
This work suggests that insoluble calcium phosphate is formed and co-precipitates any lead
present. This Interpretation is supported by animal data (see Section 10.5.2). ^
10.5.2 Animal Studies
Reports of lead-nutrient Interactions in experimental animals have generally described
such relationships in terms of a single nutrient, using relative absorption or tissue reten-
tion in the animal to index the effect. Most of the recent data are concerned with the impact
of dietary levels of calcium, iron, phosphorus, and vitamin D. Furthermore, some investigat-
ors have attempted to elucidate the site(s) of interaction as well as the mechanism(s)
NEW10A/A 10-33 7/1/83
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PRELIMINARY DRAFT
governing the interactions. Lead's Interactions involve the effect of the nutrient on lead
uptake, as well as lead's effect on nutrients; the focus of this discussion is on the former.
These interaction studies are tabulated in Table 10-4.
10.5.2.1 Interactions of Lead with Calcium. The early report of Sobel et al. (1940) noted
that variation of dietary calcium and other nutrients affected the uptake of lead by bone and
blood in animals. Subsequent studies by Mahaffey-Six and Goyer (1970) in the rat demonstrated
that a considerable reduction in dietary calcium was necessary from (0.7 percent to 0.1 per-
cent), at which level blood lead was increased 4-fold, kidney lead content was elevated 23-
fold, and relative toxicity (Mahaffey et al., 1973) was increased. The changes in calcium
necessary to alter lead's effects in the rat appear to be greater than those seen by Ziegler
et al. (1978) in young children, indicating species differences in terms of sensitivity to
basic dietary differences, as well as to levels of all interactive nutrients. These observa-
tions in the rat have been confirmed by Kostial et al. (1971), Quarterman and Morrison (1975),
Barltrop and Khoo (1975), and Barton et al. (1978a). The inverse relationship between dietary
calcium and lead uptake has also been noted in the pig (Hsu et al., 1975), horse (Willoughby
et al., 1972), lamb (Morrison et al., 1977), and domestic fowl (Berg et al., 1980).
The mechanism(s) governing lead's interaction with calcium operate at both the gut wall
and within body compartments. Barton et al. (1978a), using everted duodenal sac preparations
in the rat, reported that: (1) interactions at the gut wall require the presence of intubated
calcium to affect lead label absorption - (pre-existing calcium deficiency in the animal and
no added calcium have no effect on lead transport); (2) animals having calcium deficiency show
Increased retention of lead rather than absorption (confirmed by Quarterman et al., 1973); and
(3) lead transport may be mediated by two mucosal proteins, one of which has high molecular
weight, a high proportion of bound lead, and 1s affected in extent of lead binding with
changes in lead uptake. The second protein binds mainly calcium and is vitamin D-dependent.
Smith et al. (1978) found that lead is taken up at a different site in the duodenum of
rats than is calcium but absorption does occur at the site of phosphate uptake, suggesting a
complex interaction of phosphorus, calcium, and lead. This 1s consistent with the data of
Barltrop and Khoo (1975) for rats and the data of Heard and Chamberlain (1982) for humans,
thus showing that the combined action of the two mineral nutrients is greater than the sum of
either's effects.
MykkSnen and Wassernann (1981) observed that lead uptake in the intestine of the chick
occurs in 2 phases: a rapid uptake (within 5 minutes) followed by a rate-limiting slow trans-
fer of lead into blood. Conrad and Barton (1978) have observed a similar process in the rat.
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TABLE 10-4. EFFECT OF NUTRITIONAL FACTORS ON LEAD UPTAKE IN ANIMALS
Factor
Species
Index of effect
Interactive effect
Reference
Calcium
Calcium
Calcium
0
1
Calcium
Calcium
Iron
Iron
Iron
Rat Lead in tissues and
effect severity at
low levels of dietary
calcium
Pig Lead in tissues at
low levels of
dietary calcium
Horse Lead in tissues at
low levels of
dietary calcium
Lamb Lead in tissue at
low levels of
dietary calcium
Rat Lead retention
Rat Tissue levels and
relative toxicity
of lead
Rat Lead absorption in
everted duodenal
sac preparation
Mouse Lead retention
Low dietary calcium (0.2%)
increases lead absorption
and severity of effects
Increased absorption of
lead with low dietary
calcium
Increased absorption of
lead with low dietary
calcium
Increased absorption of
lead with low dietary
calcium
Retention increased in
calcium deficiency
Iron deficiency increases
lead absorption and
toxicity
Reduction in intubated
iron increases lead
absorption; increased
levels decrease lead uptake
Iron deficiency has no
effect on lead
retention
Mahaffey-Six and Goyer,
1970; Mahaffey et al. ,
1973
Hsu et al., 1975
Wi 1loughby et al., 1972
Morrison et al., 1977
Barton et al., 1978a
Mahaffey-Six and Goyer,
1972
Barton et al., 1978b
Hamilton, 1978
-o
30
3»
TO
•<
O
TQ
-------
Factor
Species Index of effect
Iron Rat
Phosphorus Rat
Phosphorus Rat
Phosphorus Rat
Vitamin D Rat
Vitamin D Rat
Lipid Rat
Protein Rat
In utero or milk
transfer of lead in
pregnant or lactating
rats
lead uptake in tissues
Lead retention
Lead retention
Lead absorption
using everted sac
techniques
Lead absorption
using everted sac
techniques
Lead absorption
Lead uptake by tissues
10-4. (continued)'
Interactive effect
Iron deficiency increases
both |n utero and milk
transfer of lead to
sucklings
Reduced P increased
203Pb uptake 2.7-fold
Low dietary P enhances
lead retention; no
effect on lead resorption
in bone
Low dietary P enhances
both lead retention "and
deposition in bone
Increasing vitamin D
increases intubated
lead abosrption
Both low and excess
levels of vitamin D
increase lead uptake
by affecting motility
Increases in lipid (corn
oil) content up to
40 percent enhances lead
absorption
Both low and high protein
in diet increase lead
absorption
Reference
Cerklewski, 1980
Bar!trap and Khoo, 1975
Quarter-wan and Morrison,
1975
Barton and Conrad, 1981
Smith et al., 1978
Barton et al.» 1980
Barltrop and Khoo, 1975
Barltrop and Khoo, 1975
-------
TABLE 10-4. (continued)
Factor
Species
Index of effect
Interactive effect
Reference
Protein
Rat
Body lead retention
Low dietary protein either
reduces or does not affect
retention in various
tissues
Quarterman et al., 1978b
Protein
Rat
Tissue levels of
lead
Casein in diet increases
lead uptake compared to
soybean neal
Anders et al., 1982
Milk components
Rat
Lead absorption
Lactose-hydro1yzed milk
does not increase lead
absorption, but ordinary
milk does
Bell and Spickett, 1981
Milk components
Rat
Lead absorption
Lactose in diet enhances
lead absorption compared
to glucose
Bushnell and DeLuca, 1981
Zinc/Copper
Rat
Lead absorption
Low line in diets
increases lead absorption
Cerklewski and Forbes,
1976; El-Gazzar et al.,
1978
Zinc/Copper
Rat
Lead transer in
utero and in milk
during lactation
Low-zinc diet of mother
increases lead transfer
in utero and in maternal
iiTlk
Cerklewski, 1979
Zinc/Copper
Rat
Lead absorption
Low copper in diet
increases lead absorption
Klauder et al., 1973;
Klauder and Petering, 1975
-------
PRELIMINARY DRAFT
Hence, there 1s either a saturation process occurring, I.e., carrier-mediated transport, or
simply lead precipitation in the lumen. In the former case, calcium interacts to saturate the
carrier proteins as isolated by Barton et al. (1978a) or may precipitate lead 1n the lumen by
Initial formation of calcium phosphate.
Quarterman et al. (1978a) observed that calcium supplementation of the diet above normal
also resulted in increased body retention of lead in the rat. Because both deficiency (Barton
et al., 1978a) and excess in calcium intake enhance retention, two sites of influence on
retention are suggested. Goyer (1978) has suggested that body retention of lead in calcium
deficiency, i.e., reduced excretion rate, may be due to renal impairment, while Quarter-man et
al. (1978a) suggest that excess calcium suppresses calcium resorption from bone, hence also
reducing lead release.
10.5.2.2 Interactions of Lead with Iron. Mahaffey-Six and Goyer (1972) reported that iron-
deficient rats had increased tissue levels of lead and manifested greater toxicity compared
with control animals. This uptake change was seen with but minor alterations in hematocrit,
indicating a primary change in lead absorption over the time of the study. Barton et al.
(1978b) found that dietary restriction of iron, using 210Pb and everted sac preparations in
the rat, led to enhanced absorption of iron; iron loading suppressed the extent of lead
uptake, using normal intake levels of iron. This suggests receptor binding competition at a
common site, consistent with the isolation by these workers of two iron-binding mucosa frac-
tions. While iron level of diet affects lead absorption, the effect of changes in lead con-
tent in the gut on iron absorption is not clear. Barton et al. (1978b) and Dobbins et al.
(1978) observed no effect of lead in the gut on iron absorption in the rat, while Flanagan et
al. (1979) reported that lead reduced iron absorption in mice.
In the mouse, Hamilton (1978) found that body retention of 203Pb was unaffected by iron
deficiency, using intraperitoneal administration of the label, while gastric intubation did
lead to increased retention. Animals with adequate iron showed no changes in lead retention
at intubation levels of 0.01 to 10 nM. Cerklewski (1980) observed that lead transfer both In
utero and In milk to nursing rats was enhanced when dams were maintained from gestation
through lactation on low iron diets compared with controls.
10.5.2.3 Lead Interactions with Phosphate. The early studies of Shelling (1932), Grant et
al. (1938), and Sobel et al. (1940) documented that dietary phosphate influenced the extent of
lead toxicity and tissue retention of lead in animals, with low levels enhancing those para-
meters while excess intake retarded the effects. More recently, Barltrop and Khoo (1975)
reported that reduced phosphate increased the uptake of 203Pb approximately 2.7-fold compared
with controls. Quarterman and Morrison (1975) found that low dietary phosphate enhanced lead
retention in rats but had no effect on skeletal lead mobilization nor was injected lead
label affected by such restriction. In a related study, Quarterman et al. (1978a) found that
NEW10A/A 10-38 7/1/83
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PRELIMINARY DRAFT
doubling of the nutrient over nomal levels resulted In lowering of lead absorption by appro-
ximately half. Barton and Conrad (1981) found that reduced dietary phosphorus Increased the
retention of labeled lead and deposition in bone, 1r> contrast to the results of Quarterman and
Morrison (1975). Increasing the Intraluminal level of phosphorus reduced lead absorption,
possibly by Increasing Intraluminal precipitation of lead as the mixed lead/calcium phosphate.
Smith et al. (1978) reported that lead uptake occurs at the same site as phosphate, suggesting
that lead absorption may be more related to phosphate than calcium transport.
10.5.2.4 Interactions of lead with Vitamin D. Several studies had earlier indicated that a
positive relationship might exist between dietary vitamin D and lead uptake, resulting 1n
either greater manifestations of lead toxicity or a greater extent of lead uptake (Sobel et
al., 1938, 1940). Using the everted sac technique and testing with 210Pb, Smith et al. (1978)
observed that Increasing levels of intubated vitamin D in the rat resulted in Increased
absorption of the label, with uptake occurring at the distal end of the rat duodenum, the site
of phosphorus uptake and greatest stimulation by the vitamin. Barton et al. (1980) used *10Pb
to monitor lead absorption in the rat under conditions of normal, deficient, and excess
amounts of dietary vitamin 0. lead absorption is Increased with either low or excess vitamin
D. This apparently occurs because of increased retention time of fecal mass containing the
lead due. to alteration of intestinal motility rather than because of direct enhancement of
mucosal uptake rate. Hart and Smith (1981) reported that vitamin D repletion of diet enhanced
lead absorption (210Pb) in the rat, while also enhancing femur and kidney lead uptake when the
label was given by injection.
10.5.2.5 Interactions of Lead with Lipids. Barltrop and Khoo (1975) observed that varying
the lipid (corn oil) content of rat diet from 5 up to 40 percent resulted in an Increase of
lead in blood 13.6-fold higher compared with the normal level. Concomitant increases were
observed in lead levels in kidney, femur, and carcass. Reduction of dietary lipid below the
5 percent control figure was without effect on lead absorption rate. As an extension of this
earlier work, Barltrop (1982) has noted that the chemical composition of the lipid is a signi-
ficant factor in affecting lead absorption. Study of triglycerides of saturated and unsatura-
ted fatty acids showed that polyunsaturated, trilinoleln Increased lead absorption by 80 per-
cent In rats, when given as 5 or 10 percent loadings In diet, compared with monounsaturated
triolein or any of the saturates in the series trlcaproin to tristearln.
10.5.2.6 lead Interaction with Protein. Quarterman et al. (1978b) have drawn attention to
one of the inherent difficulties of measuring lead-protein interactions, I.e., the effect of
protein on both growth and the toxlcokinetic parameters of lead. Der et al. (1974) found that
reduction of dietary protein, from 20 to 4 percent, led to increased uptake of lead in rat
tissues, but the approximately 6-fold reduction in body weight over the interval of the study
makes It difficult to draw any firm conclusions. Barltrop and Khoo (1975) found that lead
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PRELIMINARY ORAFT
(203pb) uptake by rat tissue could be enhanced with either suboptimal or excess levels of pro-
tein in diet. Quarterman et al. (1978b) reported that retention of labeled lead in rats main-
tained on a synthetic diet containing approximately 7 percent protein was either unaffected or
reduced compared with controls, depending on tissues taken for study.
It appears that not only levels of protein but also the type of protein affects tissue
levels of lead. Anders et al. (1982) found that rats maintained on either of two synthetic
diets varying only as to having casein or soybean meal as the protein source showed signifi-
cantly higher lead levels in the casein group.
10.5.2.7 Interactions of Lead with Milk Components. For many years, milk was recommended
prophylactically for lead poisoning among lead workers (Stephens and Waldron, 1975). More
recent data, however, suggest that milk may actually enhance lead uptake. Kello and Kostial
(1973) found that rats maintained on milk diets absorbed a greater amount of 203Pb than those
having access to commercial rat chow. This was ascribed to relatively lower levels of certain
nutrients in milk compared with the rat chow. These observations were confirmed by Bell and
Spickett (1981), who also observed that lactose-hydrolyzed milk was less effective than the
ordinary form in promoting lead absorption, suggesting that lactose may be the enhancing prin-
ciple. Bushnell and DeLuca (1981) demonstrated that lactose significantly increased lead
(210Pb) absorption and tissue retention by weanling rats by comparing diets Identical in all
respects except for carbohydrate source. These results provide one rationale for why nursing
mammals tend to absorb greater quantities of lead than adults; lactose is the major carbohy-
drate source in suckling rats and is known to enhance the uptake of many essential metals.
10.5.2.8 Lead Interactions with Zinc and Copper. The studies of Cerklewski and Forbes (1976)
and El-Gazzar et al. (1978) documented that zinc-deficient diets promote lead absorption in
the rat, while repletion with zinc reduces lead uptake. The interaction continues within the
body, particularly with respect to ALA-D activity (see Chapter 11). In a study of zinc-lead
Interactions in female rats during gestation and lactation, Cerklewski (1979) observed that
zinc-deficient diets resulted in more transfer of lead through milk to the pups as well as
reduced litter body weights.
Klauder et al. (1973) reported that low dietary copper enhanced lead absorption in rats
fed a high lead diet (5000 ppm). These observations were confirmed by Klauder and Petering
(1975) at a level of 500 ppm lead in diet. These researchers subsequently observed that
reduced copper enhanced the hematological effects of lead (Klauder and Petering, 1977), and
that both copper and iron deficiencies must be corrected to restore hemoglobin levels to
normal.
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I
10.6 INTERRELATIONSHIPS OF LEAD EXPOSURE, EXPOSURE INDICATORS, AND TISSUE LEAD BURDENS
Information presented so far in this chapter sets forth the quantitative and qualitative
aspects of lead toxicokinetics, including the conpartnental modeling of lead distribution in
vivo, and leads up to the critical issue of the various interrelationships of lead toxico-
kinetics to lead exposure, toxicant levels in Indicators of such exposure, and exposure-target
tissue burdens of lead.
Chapter 11 (Sections 11.4, 11.5, 11.6) discusses the various experimental and epidemiolo-
gical studies relating the relative impact of various routes of lead exposure on blood lead
levels in human subjects, including the description of mathematical models for such relation-
ships. In these sections, the basic question is: what is the mathematical relationship of
lead in air, food, water, etc. to lead in blood? This question is descriptive and does not
address the biological basis of the observed relationships. Nor does it consider the impli-
cations for adverse health risk in the sequence of exposure leading from external lead to lead
in some physiological Indicator to lead in target tissues.
For purposes of discussion, this section separately considers 1) the temporal character-
istics of physiological indicators of lead exposure, 2) the biological aspects of the rela-
tionship of external exposure to internal indicators of exposure, and 3) internal indicator-
tissue lead relationships, including both steady-state lead exposure and abrupt changes in
lead exposure. The relationship of internal indicators of body lead, such as blood lead, to
biological indicators such as EP or urinary ALA is discussed in Chapter 13, since any compara-
tive assessment of the latter should follow the chapter on biological effects, Chapter 12.
10.6.1 Temporal Characteristics of Internal Indicators of Lead Exposure
The biological half-time for blood lead or the non-retained fraction of body lead is
relatively short (see Sections 10.3 and 10.4); thus, a given blood or urine lead value
reflects rather recent exposure. In cases where lead exposure can be reliably assumed to have
occurred at a given level,, a Wood lead value Is more useful than in cases where some inter-
mittent, high level of exposure may have occurred. The former most often occurs with occupa-
tional exposure, while the latter is of particular relevance to young children.
Accessible mineralizing tissue, such as shed teeth, extend the time frame for assessing
lead exposure from weeks or several months to years (Section 10.3), since teeth accumulate
lead up to the time of shedding or extraction. Levels of lead in teeth increase with age In
proportion to exposure (Steenhout and Pourtois, 1981). Furthermore, tooth levels are propor-
tional to blood lead levels in humans (Shapiro et al., 1978) and animals (Kaplan et al.,
1980). The technique of Fremlin and Edmonds (1980), employing micro-autoradiography of
irradiated teeth, permits the identification of dentine zones high in lead content, thus
allowing the disclosure of past periods of abrupt Increases in lead intake.
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While levels of lead in shed teeth are more valuable than blood lead in assessing expo-
sure at more remote time points, such Information 1s retrospective" in nature and would not be
of use 1n monitoring current exposure. In this case, serial blood lead measurements must be
employed. With the development of methodology for in situ measurement of tooth lead in chil-
dren (described in Chapter 9), serial In situ tooth analysis in tandem with serial blood lead
determining would provide comparative data for determination of both time-concordant blood/
tooth relationships as well as which measure is the better indicator of ongoing exposure.
Given the limitations of an indicator such as blood lead in reflecting lead uptake in target
organs, as discussed below, it may well be the case that the rate of accumulation of lead in
teeth, measured i_n situ, is a better index of ongoing tissue lead uptake than is blood lead.
This aspect merits further study, especially as Shapiro et al. (1978) were able to demonstrate
the feasibility of using in situ tooth lead analysis in a large group of children screened for
lead exposure.
10.6.2 Biological Aspects of External Exposure-Internal Indicator Relationships
Information provided in Chapter 11 as well as the critique of Hammond et al. (1981) indi-
cate that the relationship of levels of lead in air, food, and water to lead in blood is
curvilinear, with the result that as "baseline" blood lead rises, i.e., as one moves up the
curve, the relative change in the dependent variable, blood lead, per unit change of lead in
some intake medium (such as air) becomes smaller. Conversely, as one proceeds down the curve
with reduction in "baseline" lead, the corresponding change in blood lead becomes larger. One
assumption in this "single medium" approach is that the baseline is not integrally related to
the level of lead in the particular medium being studied. This assumption is not necessarily
appropriate in the case of air vs. food lead, nor, in the case of young children, air lead vs.
total oral intake of the element.
Hammond et al. (1981) have noted that the shape of the blood lead curves seen in human
subjects 1s similar to that discernible in certain experimental animal studies with dogs,
rats, and rabbits (Azar et al., 1973; Prpi£-Majid et al., 1973). Also, Kimmel et al. (1980)
exposed adult female rats to lead at four levels in drinking water for 6-7 weeks and reported
values of blood lead that showed curvilinear relationship to the dose levels. Over the dosing
range of 5 to"250 ppm in water, the blood lead range was 8.5 to 31 M9/d1. In a related study
(Grant et al. , 1980) rats were exposed to lead in utero, through weaning, and up to 9 months
of age at the dosing range used in the Kimmel et al. study the weanlings, 0.5 to 250 ppm in
the dams' drinking water until weaning of pups; then the same levels in the weanlings' drink-
ing water) showed a blood lead range of 5 to 67 Mg/dl. It may be assumed in all of the above
studies that lead in the various dosing groups was near or at equilibrium within the various
body compartments.
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The biological basis of the curvilinear relationship of blood lead to lead intake does
not appear to be due to reduced absorption or enhanced excretion of the element with changes
in exposure level. In other words, a decrease in the ratio of blood lead to medium lead as
blood lead increases cannot be taken to indicate reduced uptake rate of lead into target tis-
sues. In the study of Prpic-Majid et al. (1973), dosing was by injection so that the GI
absorption rate of lead was not a factor. Azar et al. (1973) reported values for urinary lead
across the dosing groups that indicated the excretion rate for the 10, 50, 100, and 500 ppm
dietary lead groups was fairly constant. As suggested by Hammond et al. (1981), the shape of
the blood lead curves in the context of external exposure is probably related to the tissue
distribution of lead. Other supporting evidence is the relationship of blood lead to chela-
table lead and that of tissue burden to dosing level as discussed below.
10,6.3 Internal Indicator-Tissue Lead Relationships
In living human subjects it is not possible to directly determine tissue burdens of lead
(or relate these levels to adverse effects associated with target tissue) as a function of
lead intake. Instead, measurement of lead in an accessible indicator such as blood, along
with determination of some biological indicator of impairment, e.g., ALA-U or EP, is used.
Evidence continues to accumulate in both the clinical and experimental animal literature
that the use of blood lead as an indicator has limitations in reflecting both the amounts of
lead in target tissues and the temporal changes in tissue lead with changes in exposure. Per-
haps the best example of the problem is the relationship of blood lead to chelatable lead (see
Section 10.3.3). Presently, measurement of the plumburesis associated with challenge by a
single dose of a chelating agent such as CaNa2EDTA is considered the best measure of the mo-
bile, potentially toxic, fraction of body lead in children and adults (Chisolm et al., 1976;
U.S. Centers for Disease Control, 1978; Chisolm and Barltrop, 1979; Hansen et al., 1981).
Chisolm et al. (1976) have documented that the relationship of blood lead to chelatable
lead is curvilinear, such that a given incremental increase in blood lead is associated with
an increasingly larger increment of mobilizable lead. The problems associated with this cur-
vilinear relationship in exposure assessment are typified by the recent reports of Saenger et
al. (1982) concerning children and Hansen et al. (1981) concerning on adult lead workers. In
the former study, it was noted that significant percentages of children having mild to moder-
ate lead exposure, as discernible by blood lead and EP measurements, were found to have uri-
nary outputs of lead upon challenge with CaNa2EDTA qualifing them for chelation therapy under
CDC guidelines. In adult workers, Hansen et al. (1981) observed that a sizable fraction of
subjects with only modest elevations in blood lead excreted lead upon CaNa2EDTA challenge sig-
nificantly exceeding the upper end of normal. This occurred at blood lead levels of 35 pg/dl
and above.
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The biological basts for the non-linearity of the relationship between blood lead and
chelatable lead, appears in a major part, to be the existence of a sizeble pool of lead in
bone that is labile to chelation. Evidence pointing to this was summarized in Section 10.3.3.
The question of how long any lead in this compartment of bone remains labile to chelation has
been addressed by several investigators in studies of both children and adults. The question
is relevant to the issue of the utility of EDTA challenge in assessing evidence for past lead
exposure.
Chisolm et al. (1976) found that a group of adolescent subjects (N = 55; 12-22 yrs old),
who had a clinical history of lead poisoning as young children and whose mean blood lead was
22.1 pg/dl at the time of study, yielded chelatable lead values that placed them on the same
regression curve as a second group of young children with current elevations of blood lead.
The results with the adolescent subjects did not provide evidence that they might have had a
past history of lead poisoning. According to the authors, this suggests that chelatable lead
at the time of excessive exposure was not retained in a pool that remained labile to chelation
years later, but underwent subsequent excretion or transfer to the inert compartment of bone.
One problem with drawing conclusions from this study is that all of the adolescents apparently
had one or more courses of chelation therapy and were removed to housing where re-exposure
would be minimal as part of their clinical management after lead poisoning was diagnosed. One
must assume that chelation therapy removed a significant portion of the mobile lead burden and
placement in lead-free housing reduced the extent of any further exposure. The obvious
question is how would this group of adolescents compare with subjects who had excessive
chronic lead exposure as young children but who did not require or receive chelation therapy?
Former lead workers challenged with CaNa2EDTA show chelatable lead values that are sig-
nificantly above normal years after workplace exposure ceases (e.g., Alessio et al., 1976;
Prlrovskl and Teisinger, 1970). In the case of former lead workers, blood lead also remains
elevated, suggesting that the mobile lead pool in bone remains in equilibrium with blood.
The closer correspondence of chelatable lead with actual tissue lead burdens, compared to
blood lead, is also reflected in a better correlation of this parameter with such biological
Indicators of impairment as EP. Saenger et al. (1982), in the study noted above, found that
the only significant correlation with erythrocyte protoporphyrin was obtained with the jjM
Pb/mM EDTA ratio. Similarly, Alessio et al. (1976) found that EP in former lead workers was
more significantly correlated with chelatable lead than with blood lead.
Consideration of both the intake vs. blood lead and the blood lead vs. chelatable lead
curves leads to the prediction that the level of lead exposure per se is more closely related
to tissue lead burden than is blood lead; this appears to be the case in experimental animals.
Azar et al. (1973) and Grant et al. (1980) reported that levels of lead in brain, kidney, and
femur followed more of a direct proportionality with the level of dosing than with blood lead.
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Finally, there is the question of how adequately an internal Indicator such as blood lead
reflects changes in tissue burden when exposure changes abruptly. In the study of BjBrklund
et al. (1981), lead levels In both blood and brain were monitored over a 6-week period in rats
exposed to lead through their drinking water. Blood lead rose rapidly by day 1, during which
time brain lead content was only slightly elevated. After day 1, the rate of increase in
blood lead began to taper off while brain lead began to rise in a near-linear fashion up to
the end of the experiment. From day 7 to 21, blood lead increased from approximately 45 to 55
Mg/dl, while brain lead increased approximately 2-fold.
Abrupt reduction in exposure similarly appears to be associated with a more rapid
response in blood than in soft tissues, particularly brain. Goldstein and Diamond (1974)
reported that termination of intravenous administration of lead to 30-day-old rats resulted in
a 7-fold drop of lead in blood by day 7. At the same time, there was no significant decrease
in brain lead. A similar difference in brain vs. blood response was reported by Momcliovid
and Kostial (1974).
In all of the above studies, it may be seen that blood lead was of limited value in
reflecting changes in the brain, which is, for children, the significant target organ for lead
exposure. With abrupt increases in exposure level, the problem concerns a much more rapid
approach to steady-state in blood than in brain. Conversely, the biological half-time for
lead clearance from blood in the young rats of both the Goldstein and Diamond (1974) and
Momcilovid and Kostial (1974) studies was much less than it appeared to be for lead movement
from brain.
Despite the limitations in indexing tissue burden and exposure changes, blood lead
remains the one measure that can reliably demonstrate the relationship of various effects.
10.7 METABOLISM OF LEAD ALKYLS
The lower alkyl lead compounds used as gasoline additives, tetraethyl lead (TEL) and
tetramethyl lead (TML), are much more toxic, i.e., neurotoxic, on an equivalent dose basis
than inorganic lead. These agents are emitted in auto exhaust and their rate of environmental
degradation depends on such factors as sunlight, temperature, and ozone levels. There is also
some concern that organolead compounds may result from biomethylation in the environment (see
Chapter 6). Finally, there appears to be a problem with the practice among children of snif-
fing leaded gasoline. The available information dealing with metabolism of lead alkyls is
derived mainly from experimental animal studies, workers exposed to the agents and cases of
lead alkyl poisoning.
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10.7.1 Absorption of Lead Alkyls in Humans and Animals
The respiratory intake and absorption of TEL and TML in the vapor state was investigated
by Heard et al. (1979), who used human volunteers inhaling 203Pb-labeled TEL and TML. Initial
lung deposition rates were 37 and 51 percent for TEL and TML, respectively. Of these amounts,
40 percent of TEL was lost by exhalation within 48 hours, while the corresponding figure for
TML was 20 percent. The remaining fraction was absorbed. The effect of gasoline vapor on
these parameters was not investigated. In this study Mortensen (1942) reported that adult
rats inhaling TEL labeled with 203Pb (0.07-7.00 mg TEL/l) absorbed 16-23 percent of the frac-
tion reaching the alveoli. Gasoline vapor had no effect on the absorption rates.
Respiratory absorption of organolead bound to particulate matter has not been specif-
ically studied as such. According to Harrison and Laxen (1978), TEL or TML does not adher to
particulate matter to any significant extent, but the toxicologically equivalent trialkyl
derivatives, formed from photolytic dissociation or ozonolysis in the atmosphere, may do so.
10.7.1.1 Gastrointestinal Absorption. Information on the rate of absorption of lead alkyls
through the gastrointestinal tract is not available in the literature. Given the level of
gastric acidity (pH 1.0) in humans, one would expect TML and TEL to be rapidly converted to
the corresponding trialkyl forms, which are comparatively more stable (Bade and Huber, 1970).
Given the similarity of the chemical and biochemical behavior of trialkyl leads to their Group
IV analogs, the trialkyltins, the report of Barnes and Stoner (1958) that triethyl tin is
quantitatively absorbed from the GI tract indicates that triethyl and trimethyllead would be
extensively absorbed via this route.
10.7.1.2 Percutaneous Absorption of Lead Alkyls. In contrast to inorganic lead salts, both
TEL and TML are rapidly and extensively absorbed through the skin in rabbits and rats (Kehoe
and Thamann, 1931; Laug and Kunze, 1948), and lethal effects can be rapidly induced in these
animals by merely exposing the skin. Laug and Kunze (1948) observed that systemic uptake of
TEL was still 6.5 percent even though most of the TEL was seen to have evaporated from the
skin surface. The rate of passage of TML was somewhat slower than that of TEL in the study of
Davis et al. (1963); absorption of either agent was retarded somewhat when applied in gaso-
line.
10.7.2 Biotransformation and Tissue Distribution of Lead Alkyls
In order to have an understanding of the jn vivo fate of lead alkyls, it is useful to
first discuss the biotransformation processes of lead alkyls known to occur in mammalian
systems. Tetraethyl and tetramethyl lead both undergo oxidative dealkylation in mammals to
the triethyl or trimethyl metabolites, which are now accepted as the actual toxic forms of
these alkyls.
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Studies of the biochemical mechanisms for these transformations, as noted by Kimmel et
al. (1977), indicate a dealkylation mediated by a P-450 dependent mono-oxygenase system in
liver microsomes, with intermediate hydroxylation. In addition to rats (Cremer, 1959; Stevens
et al., 1960; Bolanowska, 1968), mice (Hayakawa, 1972), and rabbits (Bolanowska and
Garczyrfski, 1968) this transformation also occurs in humans accidentally poisoned with TIL
(Bolanowska et al., 1967) or workers chronically exposed to TEL (Adamiak-Ziemka and
Bolanowska, 1970).
The rate of hepatic oxidative de-ethylation of TEL in mammals appears to be rather rapid;
Cremer (1959) reported a maximum conversion rate of approximately 200 TEL/g rat liver/hour.
In comparison with TEL, TML may undergo transformation at either a slower rate (in rats) or
more rapidly (in mice), according to Cremer and Calloway (1961) and Hayakawa (1972).
Other transformation steps involve conversion of triethyl lead to diethyl form, the pro-
cess appearing to be species-dependent. Bolanowska (1968) did not report the formation of
diethyl lead in rats, while significant amounts of it are present in the urine of rabbits
(Arai et al., 1981) and humans (Chiesura, 1970). Inorganic lead is formed in various species
treated with tetraethyl lead, which may arise from degradation of the diethyl lead metabolite
or some other direct process (Bolanowska, 1968), The latter process appears to occur in rats,
as little or no diethyllead is found, whereas significant amounts of inorganic lead are
present. Formation of inorganic lead with lead alkyl exposure may account for the hematolo-
gical effects seen in humans chronically exposed to the lead alkyls (see Section 12.3),
including children who inhale leaded gasoline vapor.
Partitioning of triethyl or trimethyl lead, the corresponding active metabolites of TEL
and TML, between the erythrocyte and plasma appears to be species-dependent. Byington et al.
(1980) studied the partitioning of triethyl lead between cells and plasma in vitro using
washed human and rat erythrocytes and found that human cells had a very low affinity for the
alkyl lead while rat cells bound the alkyl lead in the globin moiety at a ratio of three mole-
cules per Hb tetramer. Similarly, it was found that injected triethyl lead was associated
with whole blood levels approximately 10-fold greater than in rat plasma. The available
literature on TEL poisoning in humans concurs, as significant plasma values of lead have been
routinely reported (Boeckx et al., 1977; Golding and Stewart, 1982). These data indicate that
the rat is a poor model to use in studying the adverse effects of lead alkyls in human sub-
jects.
The biological half-time in blood for the lead alkyls depends on whether clearance of the
tetraalkyl or trialkyl forms is being observed. Heard et al. (1979) found that 203Pb-labeled
TML and TEL inhaled by human volunteers was rapidly cleared from blood (by 10 hours), followed
by a reappearance of lead. The fraction of lead in plasma initially was quite high, approxi-
mately 0.7, suggesting tetra/trialkyl lead; but the subsequent rise in blood lead showed all
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of it essentially present in the cell, which would indicate inorganic or possibly diethyl
lead. Triethyl lead in rabbits was more rapidly cleared from the blood of rabbits (3-5 days)
than was the trimethyl form (15 days) when administered as such (Hayakawa, 1972).
Tissue distribution of lead in both humans and animals exposed to TEL and TML primarily
involves the trialkyl metabolites. Levels are highest in liver, followed by kidney, then
brain (Bolanowska et al., 1967; Grandjean and Nielsen, 1979). Nielsen et al. (1978) observed
that measurable amounts of trialkyl lead were present in samples of brain tissue from subjects
witb no known occupational exposure.
The available studies on tissue retention of triethyl or trimethyl lead provide variable
findings, Bolanowska (1968) noted that tissue levels of triethyl lead in rats were almost
constant for 16 days after a single injection of TEL. Hayakawa (1972) found that the half-
time of triethyl lead in brain was 7-8 days for rats; the half-time for trimethyl lead was
much longer. In humans, Yamamura et al. (1975) reported two tissue compartments for triethyl
lead having half-times of 35 and 100 days (Yamamura et al., 1975).
10.7.3 Excretion of Lead AlkyIs
Excretion of lead through the renal tract is the main route of elimination in various
species exposed to lead alkyls (Grandjean and Nielsen, 1979). The chemical forms of lead in
urine suggest that the differing amounts of the various forms are species-dependent. Arai et
al. (1981) found that rabbits given TEL parenterally excreted lead primarily in the form of
diethyl lead (69 percent) and inorganic lead (27 percent), triethyl lead accounting only for 4
percent. In rats, Bolanowska and Garczynski (1968) found that levels of triethyl lead were
somewhat higher in urine than was the case for rabbits. In humans, Chiesura (1970) found that
trialkyl lead never was greater than 9 percent of total lead content in workers with heavy TEL
exposure. Adamiak-Ziemka and Bolanowska (1970) reported similar data; the fraction of tri-
ethyl lead in the urine was approximately 10 percent of total lead.
The urinary rates of lead excretion in human subjects with known levels of TEL exposure
were also reported by Adamiak-Ziemka and Bolanowska (1970). In workers involved with the
blending and testing of leaded gasoline, workplace air levels of lead (as TEL) ranged from
0.037 to 0.289 mg Pb/m3 and the corresponding urine levels ranged from 14 to 49 pg Pb/1, of
which approximately 10 percent was triethyl lead.
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10.8 SUMMARY
Toxlcokinetic parameters of lead absorption, distribution, retention, and excretion con-
necting external environmental lead exposure to various adverse effects are discussed In this
section. Also considered are various Influences on these parameters, e.g., nutritional
status, age, and stage of development.
A number of specific issues in lead metabolism by animals and humans merit special focus
and these include:
1. How does the developing organism from gestation to maturity differ from the adult in
toxicokinetic response to lead Intake?
2. What do these differences 1n lead metabolism portend for relative risk for adverse
effects?
3. What are the factors that significantly change the toxlcokinetic parameters in ways
relevant to assessing health risk?
4. How do the various interrelationships among body compartments for lead translate to
assessment of internal exposure and changes In Internal exposure?
10.8.1 Lead Absorption in Humans and Animals
The amounts of lead entering the bloodstream via various routes of absorption are Influ-
enced not only by the levels of the element in a given medium but also by various physical and
chemical parameters and specific host factors, such as age and nutritional status.
10.S.1.1 Respiratory Absorption of Lead. The movement of lead from ambient air to the blood-
stream is a two-part process: deposition of some fraction of inhaled air lead in the deeper
part of the respiratory tract and absorption of the deposited fraction. For adult humans, the
deposition rate of particulate airborne lead as likely encountered by the general population
1s around 30-50 percent, with these rates being modified by such factors as particle size and
ventilation rates. It also appears that essentially all of the lead deposited in the lower
respiratory tract Is absorbed, so that the overall absorption rate is governed by the deposi-
tion rate, i.e., approximately 30-50 percent. Autopsy results showing no lead accumulation in
the lung indicate quantitative absorption of deposited lead.
All of the available data for lead uptake via the respiratory tract In humans have been
obtained with adults. Respiratory uptake of lead in children, while not fully quantifiable,
appears to be comparatively greater on a body weight basis, compared to adults. A second fac-
tor influencing the relative deposition rate in children has to do with airway dimensions.
One report has estimated that the 10-year-old child has a deposition rate 1.6- to 2.7-fold
higher than the adult on a weight basis.
It appears that the chemical form of the lead compound inhaled is not a major determinant
of the extent of alveolar absorption of lead. While experimental animal data for quantitative
assessment of lead deposition and absorption for the lung and upper respiratory tract are
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limited, available information from the rat, rabbit, dog, and nonhuman primate support the
findings that respired lead in hunans is extensively and rapidly absorbed.
10.8.1,2 Gastrointestinal Absorption of Lead. Gastrointestinal absorption of lead mainly
involves lead uptake from food and beverages as well as lead deposited in the upper respira-
tory tract which 1s eventually swallowed. It also Includes ingestion of non-food material,
primarily in children via normal mouthing activity and pica. Two issues of concern with lead
uptake from the gut are the comparative rates of such absorption in developing vs. adult
organisms, including humans, and how the relative bioavailability of lead affects such uptake.
By use of metabolic balance and isotopic (radioisotope or stable isotope) studies, var-
ious laboratories have provided estimates of lead absorption in the human adult on the order
of 10-15 percent. This rate can be significantly increased under fasting conditions to 45
percent, compared to lead ingested with food. The latter figure also suggests that beverage
letd is absorbed to a greater degree since much beverage ingestion occurs between meals.
The relationship of the chemical/biochemical form of lead in the gut to absorption rate
tat been studied, although interpretation is complicated by the relatively small amounts given
•nd the presence of various components in food already present in the gut. In general, how-
•w, chemical forms of lead or their incorporation Into biological matrices seems to have a
minimal impact on lead absorption in the human gut. Several studies have focused on the ques-
tion of differences in gastrointestinal absorption rates for lead between children and adults.
It would appear that such rates for children are considerably higher than for adults: 10-15
percent for adults vs. approximately 50 percent for children. Available data for the absorp-
tion of lead from non-food items such as dust and dirt on hands are limited, but one study has
estimated a figure of 30 percent. For paint chips, a value of about 17 percent has been esti-
mated.
Experimental animal studies show that, like humans, the adult absorbs much less lead from
the gut than the developing animal. Adult rats maintained on ordinary rat chow absorb 1 per-
cent or less of the dietary lead. Various animal species studies make it clear that the new-
born absorbs a much greater amount of lead than the adult, supporting studies showing this age
dependency in humans. Compared to an absorption rate of about 1 percent in adult rats, the
rat pup has a rate 40-50 times greater. Part, but not most, of the difference can be ascribed
to a difference in dietary composition. In nonhuman primates, infant monkeys absorb 65-85
percent of lead from the gut, compared to 4 percent for the adults.
The bioavailability of lead in the gastrointestinal (GI) tract as a factor in its absorp-
tion has been the focus of a number of experimental studies. These data show that: 1) lead
in a number of forms is absorbed about equally, except for the sulfide; 2) lead in dirt and
dust and as different chemical forms is absorbed at about the same rate as pure lead salts
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added to diet; 3) lead in paint chips undergoes significant uptake from the gut; and 4) in
some cases, physical size of particulate lead can affect the rate of GI absorption.
10.8.1.3 Percutaneous Absorption of lead. Absorption of inorganic lead compounds through the
skin is of much less significance than through the respiratory and gastrointestinal routes.
This is in contrast to the case with lead alkyIs (See Section 1.10.6). One recent study using
human volunteers and 203Pb-labeled lead acetate showed that under normal conditions, absorp-
tion approaches 0.06 percent.
10.8.1.4 Transplacental Transfer of Lead. Lead uptake by the human and animal fetus readily
occurs, such transfer going on by the 12th week of gestation in humans, with increasing fetal
uptake throughout development. Cord blood contains significant amounts of lead, correlating
with but somewhat lower than maternal blood lead levels. Evidence for such transfer, besides
lead content of cord blood, includes fetal tissue analyses and reduction in maternal blood
lead during pregnancy. There also appears to be s seasonal effect on the fetus, summer-born
children showing a trend to higher blood lead levels than those born in the spring.
10.8.2 Distribution of Lead in Humans and Animals
In this subsection, the distributional characteristics of lead in various portions of the
body—blood, soft tissue, calcified tissue, and the "chelatable" or potentially toxic body
burden—are discussed as a function of such variables as exposure history and age.
10.8.2.1 Lead in Blood. More than 99 percent of blood lead is associated with the erythro-
cyte in humans under steady-state conditions, but it is the very small fraction transported in
plasma and extracellular fluid that provides lead to the various body organs. Most ("»50 per-
cent) of erythrocyte lead is bound within the cell, primarily associated with hemoglobin (par-
ticularly HbA2), with approximately 5 percent bound to a 10,000-dalton fraction, 20 percent to
a heavier molecule, and 25 percent to lower weight species.
Whole blood lead in daily equilibrium with other compartments in adult humans appears to
have a biological half-time of 25-28 days and comprises about 1.9 mg in total lead content.
Human blood lead responds rather quickly to abrupt changes in exposure. With increased lead
intake, blood lead achieves a new value in approximately 40-60 days, while a decrease in expo-
sure may be associated with variable new blood values, depending upon the exposure history.
This dependence presumably reflects lead resorption from bone. With age, furthermore, there
appears to be little change in blood lead during adulthood. Levels of lead in blood of child-
ren tend to show a peaking trend at 2-3 years of age, probably due to mouthing activity, fol-
lowed by a decline. In older children and adults, levels of lead are sex-related, females
showing lower levels than men even at comparable levels of exposure.
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In plasma, lead is virtually all bound to albumin and only trace amounts to high weight
globulins. It is not possible to state which binding form constitutes an "active" fraction
for movement to tissues. The most recent studies of the erythrocyte-plasma relationship in
humans indicate that there is an equilibrium between these blood compartments, such that
levels in plasma rise with levels in whole blood.
10.8.2.2 Lead levels in Tissues. Of necessity, various relationships of tissue lead to expo-
sure and toxicity in humans must generally be obtained from autopsy samples. Limitations on
such data include questions of how samples represent lead behavior in the living population,
particularly with reference to prolonged illness and disease states. The adequate characteri-
zation of exposure for victims of fatal accidents is a problem, as is the fact that such
studies are cross-sectional in nature, with different age groups assumed to have had similar
exposure in the past.
10.8.2.2.1 Soft tissues. After age 20, most soft tissues in humans do not show age-related
changes, in contrast to bone. Kidney cortex shows increase in lead with age which may be
associated with formation of nuclear inclusion bodies. Absence of lead accumulation in most
soft tissues is due to a turnover rate for lead which is similar to that in blood.
Based on several autopsy studies, it appears that soft tissue lead content for individ-
uals not occupationally exposed is generally below 0.5 pg/g wet weight, with higher values for
aorta and kidney cortex. Brain tissue lead level is generally below 0.2 ppm wet weight with
no change with increasing age, although the cross-sectional nature of these data would make
changes in low brain lead levels difficult to discern. Autopsy data for both children and
adults indicate that lead is selectively accumulated in the hippocampus, a finding that is
also consistent with the reginal distribution in experimental animals.
Comparisons of lead levels in soft tissue autopsy samples from children with results from
adults indicate that such values are lower in infants than in older children, while children
aged 1-16 years had levels comparable to adult women. In one study, lead content of brain
regions did not materially differ for infants and older children compared to adults. Compli-
cating these data somewhat are changes in tissue mass with age, although such changes are less
than for the skeletal system.
Subcellular distribution of lead in soft tissue is not uniform, with high amounts of lead
being sequestered in the mitochondria and nucleus. Nuclear accumulation is consistent with
the existence of lead-containing nuclear inclusions in various species and a large body of
data demonstrating the sensitivity of mitochondria to injury by lead.
10.8.2.2.2 Mineralizing tissue. Lead becomes localized and accumulates in human calcified
tissues, i.e., bones and teeth. This accumulation in humans begins with fetal development and
continues to approximately 60 years of age. The extent of lead accumulation in bone ranges up
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to 200 ng in wen ages 60-70 years, while in women lower values have been measured. Based upon
various studies, approximately 95 percent of total body lead is lodged in the bones of human
adults, with uptake distributed over trabecular and compact bone. In the human adult, bone
lead is both the most inert and largest body pool, and accumulation can serve to maintain ele-
vated blood lead levels years after exposure, particularly occupational exposure, has ended.
Compared to the human adult, 73 percent of body lead is lodged in the bones of children,
which is consistent with other information that the skeletal system of children is more meta-
bolically active than in the adult. While the increase in bone lead across childhood is mod-
est, about 2-fold if expressed as concentration, the total accumulation rate is actually 80-
fold, taking into account a 40-fold increase in skeletal mass. To the extent that some sig*
nificant fraction of total bone lead in children and adults is relatively labile, it is more
appropriate in terms of health risk for the whole organism to consider the total accumulation
rather than just changes in concentration.
The traditional view that the skeletal system was a "total" sink for body lead (and by
implication a biological safety feature to permit significant exposure in industrialized popu-
lations) never did accord with even older information on bone physiology, e.g., bone remodel-
ling, and is now giving way to the view that there are at least several bone compartments for
lead, with different mobility profiles. It would appear, then, that "bone lead" may be more
of an insidious source of long-term internal exposure than a sink for the element. This
aspect of the issue is summarized more fully in the next section. Available information from
studies of such subjects as uranium miners and human volunteers ingesting stable isotopes
indicates that there is a relatively inert bone compartment for lead, having a half-time of
several decades, and a rather labile compartment which permits an equilibrium between bone and
tissue lead.
Tooth lead also increases with age at a rate proportional to exposure and roughly propor-
tional to blood lead in humans and experimental animals. Dentine lead is perhaps the most
responsive component of teeth to lead exposure since it is laid down from the time of eruption
until shedding. It is this characteristic which underlies the utility of dentine lead levels
in assessing long-term exposure.
10.8.2.2.3 Chelatable lead. Mobile lead in organs and systems is potentially more active
toxicologically in terms of being available to biological sites of action. Hence, this frac-
tion of total body lead burden is a more significant predictor of imminent toxicity. In
reality, direct measurement of such a fraction in human subjects would not be possible. In
this regard, "chelatable" lead, measured as the extent of plumburesis in response to admini-
stration of a chelating agent, is not viewed as the most useful probe of undue body burden in
children and adults.
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A quantitative description of the inputs to the body lead fraction that is chelant-
mobilizable is difficult to fully define, but it most likely includes a labile lead compart-
ment within bone as well as in soft tissues. Support for this view includes: 1) the age
dependency of chelatable lead, but not lead in blood or soft tissues; 2) evidence of removal
of bone lead in chelation studies with experimental animals; 3) in vitro studies of lead
mobilization in bone organ explants under closely defined conditions; 4) tracer modelling
estimates In human subjects; and 5) the complex nonlinear relationship of blood lead and lead
intake through various media. Data for children and adults showing a logarithmic relationship
of chelatable lead to blood lead and the phenomenon of "rebound" in blood lead elevation after
chelation therapy regimens (without obvious external re-exposure) offer further support.
10,8.2.2.4 Animal studies. Animal studies have been of help in sorting out some of the rela-
tionships of lead exposure to in vivo distribution of the element, particularly the impact of
skeletal lead on whole body retention. In rats, lead administration results in an initial
increase in soft tissues, followed by loss from soft tissue via excretion and transfer to
bone. Lead distribution appears to be relatively independent of dose. Other studies have
shown that lead loss from organs follows first-order kinetics except for bone, and the skele-
tal system in rats and mice is the kinetically rate-limiting step in whole-body lead clear-
ance.
The neonatal animal seems to retain proportionally higher levels of tissue lead compared
to the adult and manifests slow decay of brain lead levels while showing a significant decline
over time in other tissues. This appears to be the result of enhanced lead entry to the brain
because of a poorly developed brain barrier system as well as enhanced body retention of lead
by young animals.
The effects of such changes as metabolic stress and nutritional status on body redistri-
bution of lead have been noted. Lactating mice, for example, are known to demonstrate tissue
redistribution of lead, specifically bone lead resorption with subsequent transfer of both
lead and calcium from mother to pups.
10*8-3 Lead Excretion and Retention in Humans and Animals
10.8.3.1 Human Studies. Dietary lead in humans and animals that is not absorbed passes
through the gastrointestinal tract and is eliminated with feces, as is the fraction of air
lead that is swallowed and not absorbed. Lead entering the bloodstream and not retained is
excreted through the renal and 61 tracts, the latter via biliary clearance. The amounts
excreted through these routes are a function of such factors as species, age, and exposure
characteristics.
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Based upon the human metabolic balance data and Isotope excretion findings of various
investigators, it appears that short-term lead excretion 1n adult humans amounts to 50-60 per-
cent of the absorbed fraction, with the balance moving primarily to bone and some fraction
(approximately half) of this stored amount eventually being excreted. This overall retention
figure of 25 percent necessarily assumes that isotope clearance reflects that for body lead in
all compartments. The rapidly excreted fraction has a biological half-time of 20-25 days,
similar to that for lead removal from blood. This similarity indicates a steady rate of lead
clearance from the body. In terms of partitioning of excreted lead between urine and bile,
one stu<{y indicates that the biliary clearance is about 50 percent that of renal clearance.
Lead is accumulated in the human body with age, mainly in bone, up to around 60 years of
age, when a decrease occurs with changes in intake as well as in bone mineral metabolism. As
noted earlier, the total amount of lead in long-term retention can approach 200 mg, and even
much higher in the case of occupational exposure. This corresponds to a lifetime average
retention rate of 9-10 M9 Pg/day. Within shorter time frames, however, retention will vary
considerably due to such factors as development, disruption in the individuals' equilibrium
with lead intake, and the onset of such states as osteoporosis.
The age dependency of lead retention/excretion in humans has not been well studied, but
most of the available information indicates that children, particularly infants, retain a sig-
nificantly higher amount of lead. While autopsy data indicate that pediatric subjects at iso-
lated points in time actually have a lower fraction of body lead lodged in bone, a full under-
standing of longer-term retention over childhood must consider the exponential growth rate oc-
curring in a child's skeletal system over the time period for which bone lead concentrations
have been gathered. This parameter itself represents a 40-fold mass increase. This signifi-
cant skeletal growth rate has an impact on an obvious question: if children take in more lead
on a body weight basis than adults, absorb and retain more lead than adults, and show only
modest elevations 1n blood lead compared to adults 1n the face of a more active skeletal sys-
tem, where does the lead go? A second factor is the assumption that blood lead in children
relates to body lead burden in the same quantitative fashion as in adults, an assumption that
remains to be adequately proven.
10.8.3.2 Animal Studies. In rats and other experimental animals, both urinary and fecal
excretion appear to be important routes of lead removal from the organism; the relative parti-
tioning between the two modes 1s species- and dose-dependent. With regard to species differ-
ences, biliary, clearance of lead in the dog 1s but 2 percent of that for the rat, while such
excretion in the rabbit is 50 percent that of the rat.
Lead movement from laboratory animals to their offspring via milk constituents is a route
of excretion for the mother as well as an exposure route for the young. Comparative studies
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of lead retention 1n developing vs. adult animals, e.g., rats, nice, and non-human primates,
make it clear that retention is significantly greater in the young animal. These observations
support those studies showing greater lead retention in children. Some recent data indicate
that a differential retention of lead in young rats persists into the post-weaning period,
calculated as either uniform dosing or uniform exposure.
10.8.4 Interactions of Lead with Essential Metals and Other Factors
Toxic elements such as lead are affected in their toxicokinetic or toxicological behavior
by interactions with a variety of biochemical factors such as nutrients.
10.8.4.1 Human Studies. In humans the interactive behavior of lead and various nutritional
factors is expressed most significantly in young children, with such interactions occurring
against a backdrop of rather widespread deficiencies in a number of nutritional components.
Various surveys have indicated that deficiency in iron, calcium, zinc, and vitamins are wide-
spread among the pediatric population, particularly the poor. A number of reports have docu-
mented the association of lead absorption with suboptimal nutritional states for iron and cal-
cium, reduced intake being associated with increased lead absorption.
10.8.4.2 Animal Studies. Reports of lead-nutrient interactions in experimental animals have
generally described such relationships for a single nutrient, using relative absorption or
tissue retention in the animal to Index the effect. Most of the recent data are for calcium,
iron, phosphorus, and vitamin D. Many studies have established that diminished dietary calci-
um is associated with increased blood and soft tissue lead content in such diverse species as
the rat, pig, horse, sheep, and domestic fowl. The increased body burden of lead arises from
both Increased GI absorption and increased retention, indicating that the lead-calcium inter-
action operates at both the gut wall and within body compartments. Lead appears to traverse
the gut via both passive and active transfer, involves transport proteins normally operating
for calcium transport, and 1s taken up at the site of phosphorus, not calcium, absorption.
Iron deficiency is associated with an increase in lead of tissues and Increased toxicity,
an effect which is expressed at the level of lead uptake by the gut wall. In v**ro studies
Indicate an interaction through receptor binding competition at a common site. This probably
involves iron-binding proteins. Similarly, dietary phosphate deficiency enhances the extent
of lead retention and toxicity via increased uptake of lead at the gut wall, both lead and
phosphate being absorbed at the same site in the small intestine. Results of various studies
of the resorption of phosphate along with lead as one further mechanism of elevation of tissue
lead have not been conclusive. Since calcium plus phosphate retards lead absorption to a
greater degree than simply the sums of the Interactions, it has been postulated that an insol-
uble complex of all these elements may be the basis of this retardation.
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Unlike the Inverse relationship existing for calcium, iron, and phosphate vs. lead
uptake, vitamin D levels appear to be directly related to the rate of lead absorption from the
GI tract, since the vitamin stimulates the sane region of the duodenum where lead is absorbed.
A number of other nutrient factors are known to have an interactive relationship with lead:
1. Increases in dietary lipids increase the extent of lead absorption, with the extent
of the Increase being highest with polyunsaturates and lowest with saturated fats,
e.g., tristearin.
2. The interactive relationship of lead and dietary protein is not clearcut, and either
suboptinal or excess protein intake will increase lead absorption.
3. Certain milk components, particularly lactose, will greatly enhance lead absorption
in the nursing animal.
4. Zinc deficiency promotes lead absorption as does reduced dietary copper.
10.8.5 Interrelationships of Lead Exposure with Exposure Indicators and Tissue lead Burdens
There are three issues involving lead toxicokinetics which evolve toward a full connec-
tion between lead exposure and its adverse effects; 1) the temporal characteristics of inter-
nal indices of lead exposure; 2) the biological aspects of the relationship of lead in vari-
ous media to various indicators in internal exposure; and 3) the relationship of various
internal indicators of exposure to target tissue lead burdens.
10.8.5.1 Temporal Characteristics of Internal Indicators of Lead Exposure. The biological
half-time for newly absorbed lead in blood appears to be of the order of weeks or several
months, so that this medium reflects relatively recent exposure. If recent exposure is fairly
representative of exposure over a considerable period of time, e.g., exposure of lead workers,
then blood lead is more useful than for cases where exposure is intermittent or different
across time, as in the case of lead exposure of children. Accessible mineralized tissue, such
as shed teeth, extend the time frame back to years of exposure, since teeth accumulate lead
with age and as a function of the extent of exposure. Such measurements are, however, retro-
spective in nature, in that identification of excessive exposure occurs after the fact and
thus limits the possibility of timely medical intervention, exposure abatement, or regulatory
policy concerned with ongoing control strategies.
Perhaps the most "practical solution to the dilemma posed by both tooth and blood lead
analyses is in situ measurement of lead in teeth or bone during the time when active accumu-
lation occurs, e.g., 2-3-year-old children. Available data using X-ray fluorescence analysis
do suggest that such approaches are feasible and can be reconciled with such issues as accept-
able radiation hazard risk to subjects.
10.8.5.2 Biological Aspects of External Exposure-Internal Indicator Relationships. It is
m mm • ¦ — 11 ¦
clear from a reading of the literature that the relationship of lead in relevant media for
human exposure to blood lead is curvilinear when viewed over a relatively broad range of blood
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lead values. This implies that the unit change in blood lead per unit intake of lead in some
medium varies across this range of exposure, with comparatively smaller blood lead changes as
internal exposure increases.
Given our present knowledge, such a relationship cannot be taken to mean that body uptake
of lead is proportionately lower at higher exposure, for it may simply mean that blood lead
becomes an increasingly unreliable measure of target tissue lead burden with increasing expo-
sure. While the basis of the curvilinear relationship remains to be identified, available
animal data suggest that it does not reflect exposure-dependent absorption or excretion rates.
10.8.5.3 Internal Indicator-Tissue lead Relationships. In living human subjects, it is not
possible to directly determine tissue lead burdens or how these relate to adverse effects in
target tissues; some accessible indicator, e.g., lead in a medium such as blood or a biochem-
ical surrogate of lead such as EP, must be employed. While blood lead still remains the only
practical measure of excessive lead exposure and health risk, evidence continues to accumulate
that such an index has limitations in either reflecting tissue lead burdens or changes in such
tissues with changes in exposure.
At present, the measurement of plumburesis associated with challenge by a single dose of
a lead chelating agent such as CaNa2EDTA is considered the best indicator of the mobile,
potentially toxic fraction of body lead. Chelatable lead is logarithmically related to blood
lead, such that incremental increase in blood lead is associated with an increasingly larger
increment of mobilizable lead. The problems associated with this logarithmic relationship may
be seen in studies of children and lead workers in whom moderate elevation in blood lead can
disguise levels of mobile body lead. This reduces the margin of protection against severe
intoxication. The biological basis of the logarithmic chelatable lead-blood lead relationship
rests, in large measure, with the existence of a sizable bone lead compartment that is mobile
enough to undergo chelation removal and, hence, potentially mobile enough to move into target
tissues.
Studies of the relative mobility of chelatable lead over time indicate that, in former
lead workers, removal from exposure leads to a protracted washing out of lead (from bone
resorption of lead) to blood and tissues, with preservation of a bone burden amenable to sub-
sequent chelation. Studies with children are inconclusive, since the one investigation
directed to th'is end employed pediatric subjects who all underwent chelation therapy during
periods of severe lead poisoning. Animal studies demonstrate that changes in blood lead with
increasing exposure do not agree with tissue uptake in a time-concordant fasion, nor does
decrease in blood lead with reduced exposure signal a similar decrease in target tissue, par-
ticularly in the brain of the developing organism.
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10.8.6 Metabolism of Lead Alkyls
The lower alkyl lead components used as gasoline additives, tetraethyl lead (TEL) and
tetramethyl lead (THL), may themselves poise a toxic risk to humans. In particular, there is
among children a problem of sniffing leaded gasoline.
10.8.6.1 Absorption of Lead Alkyls in Humans and Animals. Human volunteers inhaling labeled
TEL and TML show lung deposition rates for the lead alkyls of 37 and 51 percent, respectively,
values which are similar to those for particulate inorganic lead. Significant portions of
these deposited amounts were eventually absorbed. Respiratory absorption of organolead bound
to particulate matter has not been specifically studied as such.
While specific data for the GI absorption of lead alkyls in humans and animals are not
available, their close similarity to organotin compounds, which ire quantitatively absorbed,
would argue for extensive GI absorption. In contrast to inorganic lead salts, the lower lead
alkyls are extensively absorbed through the skin and animal data show lethal effects with per-
cutaneous uptake as the sole route of exposure.
10.8.6.2 Biotransformation and Tissue Distribution of Lead Alkyls. The lower lead alkyls TEL
and TML undergo monodealkylation in the liver of mammalian species via the P-450-dependent
mono-oxygenase enzyme system. Such transformation is very rapid. Further transformation
involves conversion to the dialkyl and inorganic lead forms, the latter accounting for the
effects on heme biosynthesis and erythropoiesis observed in alkyl lead intoxication. Alykl
lead is rapidly cleared from blood, shows a higher partitioning into plasma than inorganic
lead with triethyl lead clearance being more rapid than the methyl analog.
Tissue distribution of alkyl lead in humans and animals primarily involves the trialkyl
metabolites. Levels are highest in liver, followed by kidney, then brain. Of interest is the
fact that there are detectable amounts of trialkyl lead from autopsy samples of human brain
even in the absence of occupational exposure. In humans, there appear to be two tissue com-
partments for triethyl lead, having half-times of 35 and 100 days.
10.8.6.3 Excretion of Lead Alkyls. With alkyl lead exposure, excretion of lead through the
renal tract is the main route of elimination. The chemical forms :t»edng excreted appear to be
species-dependent. In humans, trialkyl lead in workers chronically exposed to alkyl lead 1s a
minor component of urine lead, approximately 9 percent.
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I
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11. ASSESSMENT OF HAD EXPOSURES AND ABSORPTION IN HUMAN POPULATIONS
11.1 INTRODUCTION
The purpose of this chapter is to describe effects on internal body burdens of lead in
human populations resulting from exposure to lead in their environment. This chapter dis-
cusses changes in various internal exposure indices that follow changes in external lead
exposures. The main index of internal lead exposure focused on herein is blood lead
levels, although other indices, such as levels of lead in teeth and bone are also briefly dis-
cussed. As noted in Chapter 10, blood lead levels most closely reflect recent exposures to
environmental lead. On the other hand, teeth and bone lead levels better reflect or index
cumulative exposures.
The following terns and definitions will be used in this chapter. Sources of lead are
those components of the environment (e.g., gasoline combustion, smelters) from which signifi-
cant quantities of lead are released into various environmental media of exposure. Environ-
mental media are direct routes by which humans become exposed to lead {e.g., air, soil, water,
dust). External exposures are levels at which lead is present in any or all of the environ-
mental media. Internal exposures are the amounts of lead present at various sites within the
bocjy.
The present chapter is organizationally structured so as to achieve the following four
Min objectives:
(1) Elucidation of patterns of absorbed lead in U.S. populations and identifi-
cation of important demographic covariates.
(2) Characterization of relationships between external and internal exposures
by exposure medium (air, food, water or dust).
(3) Identification of specific sources of lead which result in increased
internal exposure levels.
(4) Estimation of the relative contributions of various sources of lead in the
environment to total internal exposure.
The existing scientific literature must be examined in light of the Investigators' own
objectives and the quality of the scientific investigations performed. Although all studies
need to be evaluated in regard to their methodology, the more quantitative studies are evalu-
ated here in greater depth. A discussion of the main types of methodological points con-
sidered in such evaluations is presented in Section 11.2.
After discussing methodological aspects, patterns of internal exposure to lead 1n human
populations are delineated in Section 11.3. This begins with a brief examination of the
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historical record of internal lead exposure in human populations. These data serve as a back-
drop against which recent U.S. levels can be contrasted and defines the relative magnitude of
external lead exposures in the past and present. The contrast is structured as follows; his-
torical data, recent data from populations thought to be isolated from urbanized cultures, and
then U.S. populations showing various degrees of urbanization and industrialization.
Recent patterns of internal exposure in U.S. populations are discussed in greater detail.
Estimates of internal lead exposure and identification of demographic covariates are made.
Studies examining the recent past for evidence of change In levels in internal exposure are
presented." A discussion follows regarding exposure covariates of blood lead levels in urban
U.S. children, who are at special risk for increased internal exposure.
The statistical treatment of distributions of blood lead levels in human populations is
the next topic discussed. As part of that discussion, the empirical characteristics of blood
lead distributions in well defined homogeneous populations are denoted. Important issues
addressed include the proper choice of estimators of central tendency and dispersion, estima-
tors of percentile values and the potential influence Of errors in measurement on statistical
estimation involving blood lead data.
Section 11.4 focuses on general relationships between external exposures and levels of
internal exposure. The distribution of lead in man is diagramatically depicted by the compo-
nent model shown in Figure 1. Of particular importance for this document is the relationship
between lead in air and lead in blood. If lead in air were the only medium of exposure, then
the interpretation of a statistical relationship between lead in air and lead in blood would
.be relatively simple. However, this is not the case. Lead is present in a number of environ-
mental media, as described in Chapter 7 and summarized in Figure 11-1. There are relation-
ships between lead levels in air and lead concentrations in food, soil, dust and water. As
shown in Chapters 6, 7 and 8, lead emitted into the atmosphere ultimately comes back to con-
taminate the earth. However, only limited data are currently available that provide a quan-
titative estimate of the magnitude of this secondary lead exposure. The implication is that
an analysis involving estimated lead levels in all environmental media may produce an under-
estimate of the relationship between lead in blood and lead in air.
The discussion of relationships between external exposure and internal absorption com-
mences with air lead exposures. Both experimental and epidemiological studies are discussed.
Several studies are identified as being of most importance in determining the quantitative
relationship between lead in blood and lead in air. The shape of the relationship between
blood lead and air lead is of particular interest and importance.
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AUTO
EMISSIONS
INDUSTRIAL
EMISSIONS
CRUSTAL
WEATHERING
SURFACE AND
GROUND WATER
PLANTS
INHALED
AIR
DRINKING
WATER
DUSTS
FOOD
BLOOD
SOFT
TISSUE
\
KIDNEY
FECES URINE
BONES
Figure 11-1. Pathways of lead from the environment to man.
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After discussion of air lead vs. blood lead relationships, the chapter next discusses the
relationship of blood lead to atmospheric lead found in other environmental media. Section
11.5 describes studies of specific lead exposure situations useful in identifying specific
environmental sources of lead that contribute to elevated body burdens of lead. The chapter
concludes with a summary of key information and conclusions derived from the scientific evi-
dence reviewed.
11.2 METHODOLOGICAL CONSIDERATIONS
11.2.1 Analytical Problems
Internal lead exposure levels in human populations have been estimated by analyses of a
variety of biological tissue matrices (e.g., blood, teeth, bone, and hair). Lead levels in
each of these matrices have particular biological meanings with regard to external exposure
status; these relationships are discussed in Chapter 10. The principal internal exposure
Index discussed in this chapter 1s blood lead concentration. Blood lead concentrations
are most reflective of recent exposure to lead and bear a consistent relationship to levels of
lead in the external environment if the latter have been stable. Blood lead levels are vari-
ously reported as Mfl/100 9» Mfl/100 nl, pg/dl, ppm, ppb, and pm/l. The first four measures are
roughly equivalent, whereas ppb values are simply divisible by 1000 to be equivalent. Actual-
ly there is a small but not meaningful difference in blood lead levels reported on a per
volume vs. per weight difference. The difference results from the density of blood being
slightly greater than 1 g/ml. For the purposes of this chapter, data reported on a weight or
volume basis are considered equal. On the other hand, blood lead data reported on a pmol/1
basis must be multiplied by 20.72 to get the equivalent MS/dl value. Data reported originally
as ninol/1 in studies reviewed here are converted to yg/dl in subsequent sections of this
chapter.
As discussed in Chapter 9, the measurement of lead in blood has been accomplished via a
succession of analytical procedures over the years. The first reliable analytical methods
available were wet chemistry procedures that have been succeeded by increasingly automated in-
strumental procedures. With these changes in technology there has been increasing recognition
of the importance of controlling for contamination in the sampling and analytical procedures.
These advances, as well as institution of external quality control programs, have resulted in
markedly improved analytical results. Data summarized in Chapter 9 show that a generalized
improvement in analytical results across many laboratories occurred during Federal Fiscal
Years 1977 to 1979. No futher marked Improvement was seen during Federal Fiscal Years 1979 to
1981.
As difficult as getting accurate blood lead determinations is, the achievement of accu-
rate lead isotopic determinations is even more difficult. Experience gained from the isotopic
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lead experiment (ILE) in Italy (reviewed in detail 1 ft Section 11,5.1.1.1) has indicated that
extremely aggressive quality control and contamination control programs must be implemented to
achieve acceptable results. With proper procedures, meaningful differences on the order of a
single nanogram are achievable.
11.2.2 Statistical Approaches
Many studies summarize the distribution of lead levels in humans. These studies usually
report measures of central tendency (means) and dispersion (variances). In this chapter, the
term "mean" refers to the arithmetic mean unless stated otherwise. This measure Is always an
estimate of the average value, but it estimates the center of the distribution (50th percen-
tile) only for symmetric distributions. Many authors provide geometric means, which estimate
the center of the distribution if the distribution is lognormal. Geometric means are influ-
enced less by unusually large values than are arithmetic means. A complete discussion of the
lognormal distribution is given by AitcMson"and Brown (1966), including formulas for conver-
ting from arithmetic to geometric means.
Most studies also give sample variances or standard deviations in addition to the means.
If geometric means are given, then the corresponding measure of dispersion is the geometric
standard deviation. Aitchison and Brown (1966) give formulas for the geometric standard devi-
ation and, also, explain how to estimate percentiles and construct confidence Intervals. All
of the measures of dispersion actually include three sources of variation; population varia-
tion, measurement variation and variation due to sampling error. Values for these components
are needed in order to evaluate a study correctly.
A separate Issue is the form of the distribution of blood lead values. Although the nor-
mal and lognormal distributions are commonly used, there are many other possible distribu-
tions. The form is important for two reasons: 1) it determines which is more appropriate,
the arithmetic or geometric mean, and 2) it determines estimates of the fraction of a popula-
tion exceeding given internal lead levels under various external exposures. Both of these
questions arise in the discussion of the distribution of human blood lead levels.
Many studies attempt to relate blood lead levels to an estimate of dose such as lead
levels in air. Standard regression techniques should be used with caution, since they assume
that the dose variable is measured without error. The dose variable is an estimate of the
actual lead Intake and has inherent inaccuracies. As a result, the slopes tend to be under-
estimated; however, it 1s extremely difficult to quantify the actual amount of this bias.
Multiple regression analyses have additional problems. Many of the tovariates that measure
external exposures are highly correlated with each other. For example, much of the soil lead
and house dust lead comes from the air. The exact effect of such high correlations with each
other on the regression coefficients 1s not clear.
PB11A2/B 11-5 7/29/83
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11.3 LEAD IN HUMAN POPULATIONS
11.3.1 Introduction
This section is designed to provide insight into current levels of lead absorption in the
U.S. and other countries, and how they differ from "natural" levels, to examine the Influence
of demographic factors, and to describe the degree of internal exposure in selected population
subgroups. This section will also examine time trend studies of blood lead levels.
11.3.2 Ancient and Remote Populations
A question of major interest in understanding environmental pollutants is the extent to
which current ambient exposures exceed background levels. Because lead is a naturally occur-
ring element it can be surmised that some level has been and will always be present in the
human body; the question of Interest is what is the difference in the levels of current sub-
groups of the United States population from those "natural" levels. Information regarding this
issue has been developed from studies of populations that lived in the past and populations
that currently live in remote areas far from the influence of industrial and urban lead ex-
posures.
Man has used lead since antiquity for a variety of purposes. These uses have afforded
the opportunity for some segments of the human population to be exposed to lead and subse-
quently absorb it into the body. Because lead accumulates over a lifetime in bones and teeth
and because bones and teeth stay intact for extremely long times, it is possible to estimate
the extent to which populations in the past have been exposed to lead.
Because of the problems of scarcity of samples and little knowledge of how representative
the samples are of conditions at the time, the data from these studies provide only rough es-
timates of the extent of absorption. Further complicating the interpretation of these data
are debates over proper analytical procedures and the question of whether skeletons and teeth
pick up or release lead from or to the soil in which they are interred.
Despite these difficulties, several studies provide data by which to estimate internal
exposure patterns among ancient populations, and some studies have included data from both
past and current populations for comparisons. Figure 11-2, which 1s adapted from Angle (1982)
displays a historical view of the estimated lead usage and data from ancient bone and teeth
lead levels. There is a reasonably good fit. There appears to be an increase in both lead
usage and absorption over the time span covered. Specifics of these studies of bone and teeth
will be presented in Section 11.3.2.1. In contrast to the study of ancient populations using
bone and teeth lead levels, several studies have looked at the issue of lead contamination
from the perspective of comparing current remote and urbanized populations. These studies
have used blood lead levels as an indicator and found mean blood concentrations in remote
PB11A2/B
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PRELIMINARY DRAFT
i—i—i—r~i—i—i—[ /T\ i
a
o
~
ISO Z
USE OF
SILVER COINS
CO
too 3
NEW
WORLD
SILVER
DEPLETION OF
ROMAN MINES
OF
ROME
ATHENS
PERU
EGYPT
NUBIA
DENMARK
BRITAIN-ROMAN,
ANGLO- SAXON
U.S.
BRITAIN
WORLDWIDE LEAD
PRODUCTION
LEAD CONCENTRATION
IN BONES
S600 MOO
BP
4600 4000 3600 3000 2600 2000 1500 1000 GOO PRESENT
YEARS BEFORE PRESENT
Figure 11-2, Estimate of world-wide lead production arid lead concentrations
in bones l^g/gm) from 5500 years before present to the present time.
Source: Adapted from Angle and Mclntire (1982).
PB11A2/B
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PRELIMINARY DRAFT
populations between 1 and 5 pg/dl, which is an order of magnitude below current U.S. urban
population means. These studies are presented in detail in Section 11.3.2.2.
11.3.2.1 Ancient Populations. Table 11-1 presents summaries of several studies that analyzed
bones and teeth to yield approximate estimates of lead absorption in the past. Some of these
studies also analyzed contemporary current samples so that a comparison between past and pre-
sent could be made.
Samples from the Sudan (ancient Nubians) were collected from several different periods
(Grandjean et al., 1978). The oldest sample (3300-2900 B.C.) averaged 0.6 pg/g for bone and
0.9 pg/g for teeth. Data from the later time of 1650-1350 B.C. show a substantial increase in
absorbed lead. Comparison of even the most recent ancient samples with a current Danish sam-
ple show a 4- to 8-fold increase over time.
Similar data were also obtained from Peruvian and Pennsylvania samples (Becker et al.,
1968). The Peruvian and Pennsylvania samples were approximately from the same era (^1200-1400
A.D.). Little lead was used in these cultures as reflected by chemical analysis of bone lead
content. The values were less than 5 pg/g for both samples. In contrast, modern samples from
Syracuse, New York, ranged from 5 to 110 pg/g.
Fosse and Wesenberg (1981) reported a study of Norwegian samples from several eras. The
oldest material was significantly lower in lead than modern samples. Ericson et al. (1979)
also analyzed bone specimens from ancient Peruvians. Samples from 4500-3000 years ago to
about 1400 years ago were reasonably constant (<0.2 pg/g).
Aufderheide et al. (1981) report a study of 16 skeletons from colonial America. Two
social groups, identified as plantation proprietors and laborers, had distinctly different
diet exposures to lead as shown by the analyses of the skeletal samples. The proprietor
group averaged 185 pg/g bone ash while the laborer group averaged 35 pg/g.
Shapiro et al. (1975) report a study that contrasts teeth lead content of ancient popula-
tions with that of current remote populations and, also, with current urban populations. The
ancient Egyptian samples (1st and 2nd millenia) exhibited the lowest teeth lead levels, mean
of 9.7 pg/g. The more recent Peruvian Indian samples (12th Century) had similar levels
(13.6 pg/g). The contemporary Alaskan Eskimo samples had a mean of 56,0 pg/g while
Philadelphia samples had a mean of 188.3 pg/g. These data suggest an increasing pattern of
lead absorption from ancient populations to current remote and urban populations.
11.3.2.2 Remote Populations. Several studies have looked at the blood lead levels in current
remote populations (Piomelli et al., 1980; Poole and Smythe, 1980). These studies are impor-
tant in defining the baseline level of internal lead exposures found in the world today.
PB11A2/8
11-8
7/29/83
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PRELIMINARY DRAFT
TABLE 11-1. STUDIES OF PAST EXPOSURES TO LEAD
Index of
Population
Age of
Exposure
Method of
Lead
Studied
Sample
Used
Analysis
Levels
Pb
Nubians1
Mfl/a dry wt.
3300 B.C. to 750 A.D.
Teeth
FASS
Bone Tooth
vs. Modern
(5000 yrs. old)
(circum-
ASV
Danes
pupil
Nubians
dentine)
A-group
3300 to 2900 B.C.
Bone (temporal)
0.6
0.9
C-group
2000 to 1600 B.C.
1.0
2.1
Pharonic
1650 to 1350 B.C.
2.0
5.0
Merotic,
X-group &
Christians
1 to 750 A.D.
1.2
3.2
Danes
Contemporary
5.5
25.7
Bone
ug/g
Ancient
500-600 yrs. old
Bone
Arc emission
Peruvians2
(Tibia)
spectroscopy
Peru
<5
Ancient Penn-
500 yrs. old
(Femur)
sylvanian .
Penn.
N.D.
Indians
Recent
Contemporary
Modern 110, 75,
Syracuse,NY
5, 45, 16
Tooth
Uvdal3
Buried from before
Teeth
^ Ann1' ¦
mis
1200 A.D. to 1804
(Whole
1.22
Modern
Contemporary
teeth, but
4.12
Buskend County
values
Bryggen
7
corrected for
1.81
(medieval Sergen)
enamel and
Norway
Contemporary
dentine)
3.73
1Grandjean, P.; Nielsen, O.V.; Shapiro, I.M. (1978) Lead retention in ancient Nubian and
contemporary populations. J. Environ. Pathol. Toxicol. 2: 781-787.
2Becker, R.O.; Spadaro, J.A.; Berg, E.W. (1968) The trace elements in human bone. J. Bone
Jt. Surg. 50A: 326-334.
3Fosse, G.; Wesenberg, G.B.R. (1981) Lead, cadmium, line and copper in deciduous teeth of
Norwegian children in the pre-industrial age. Int. J. Environ. Stud. 16: 163-170.
PB11A2/B 11-9 7/29/83
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Piomelli et al. (1980) report a study of blood lead levels of natives in a remote (far
from industrialized regions) section of Nepal. Portable air samplers were used to determine
the air lead exposure in the region. The lead content of the air samples proved to be less
3
than the detection limit, 0.004 pg/m . A later study by Davidson et al. (1981) from Nepal
confirmed the low air lead levels reported by Piomelli et al. (1980). Davidson et al. (1981)
3
found an average air lead concentration of 0.00086 pg/m .
Blood lead levels reported by Piomelli et al. (1980) for the Nepalese natives were low;
the geometric mean blood lead for this population was 3.4 pg/dl. Adult males had a geometric
mean of 3.8 pg/dl and adult females, 2.9 fig/dl. Children had a geometric mean blood lead of
3.5 pg/dl. Only 10 of 103 individuals tested had a blood lead level greater than 10 pg/dl.
The blood samples, which were collected on filter paper discs, were analyzed by a modification
of the Delves Cup Atomic Absorption Spectrophotometry method. Stringent quality control pro-
cedures were followed for both the blood and air samples.
To put these Nepalese values in perspective, Piomelli et al. (1980) reported analyses of
blood samples collected and analyzed by the same methods from Manhattan, New York. New York
blood leads averaged about 15 yg/dl, a 5-fold increase over the Nepalese values.
Poole and Smythe (1980) reported another study of a remote population, using contam-
ination-free micro-blood sampling and chemical analysis techniques. They reported acceptable
precision at blood lead concentrations as low as 5 pg/dl, using spectrophotometry. One hun-
dred children were sampled from a remote area of Papua, New Guinea. Almost all of the chil-
dren came from families engaging in subsistence agriculture. The children ranged from 7 to 10
years and included both sexes. Blood lead levels ranged from 1 to 13 pg/dl with a mean of
5.2. Although the data appear to be somewhat skewed to the right, they are in good agreement
with those of Piomelli for Nepalase subjects.
11.3.3 Levels of Lead and Demographic Covariates in U.S. Populations
11.3.3.1 The NHANES II Study. The National Center for Health Statistics has provided the
best currently available picture of blood lead levels among United States residents as part of
the second National Health and Nutrition Examination Study (NHANES II) conducted from February
1976 to February 1980 (Mahaffey et al., 1982; McDowell et al., 1981; Annest et al., 1982).
These are the first national estimates of lead levels in whole blood from a representative
sample of the non-institutionalized U.S. civilian population aged 6 months to 74 years of age.
From a total of 27,801 persons identified through a stratified, multi-stage probability
cluster sample of households throughout the U.S., blood lead determinations were scheduled for
16,563 persons including all children ages 6 months to 6 years, and one-half of all persons
ages 7 to 74. Sampling was scheduled in 64 sampling areas over the 4-year period according to
PB11A2/B
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7/29/83
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PRELIMINARY DRAFT
a previously determined itinerary to maximize operational efficiency and response of partici-
pants. Because of the constraints of cold weather, the examination trailers traveled in the
moderate climate areas during the winter, and the more northern areas during the summer
(McDowell et al., 1981).
ATI reported blood lead levels were based on samples collected by venipuncture. Blood
lead levels were determined by atomic absorption spectrophotometry using a modified Delves Cup
micro-method. Specimens were analyzed in duplicate, with both determinations done independ-
ently in the same analytical run. Quality control was maintained by two systems, a bench
system and a blind insertion of samples. If the NHANES II replicates differed by more than
7 MQ/dl, the analysis was repeated for the specimen (about 0.3 percent were reanalyzed). If
the average of the replicate values of either "bench" or "blind" control specimens fell out-
side previously established 95 percent confidence limits, the entire run was repeated. The
estimated coefficient of variation for the "bench" quality control ranged from 7 to 15 percent
(Mahaffey et al., 1979).
The reported blood lead levels were based on the average of the replicates. Blood lead
levels and related data were reported as population estimates; findings for each person were
inflated by the reciprocal of selection probabilities, adjusted to account for persons who
were not examined and poststratified by race, sex and age. The final estimates closely
approximate the U.S. Bureau of Census estimates for the civilian non-institutionalized popula-
tion of the United States as of March 1, 1978, aged 1/2 to 74 years.
Participation rates varied across age categories; the highest non-response rate (51
percent) was for the youngest age group, 6 months through 5 years. Among medically examined
persons, those with missing blood lead values were randomly distributed by race, sex, degree
of urbanization and annual family income. These data are probably the best estimates now
available regarding the degree of lead absorption in the general United States population.
Forthofer (1983) has studied the potential effects of non-response bias in the NHANES II
survey and found no large biases in the health variables. This was based on the excellent
agreement of the NHANES II examined data, which had a 27 percent non-response rate, with the
National Health Interview Survey data, which had a 4 percent non-response rate.
The national estimates presented below are based on 9,933 persons whose blood lead levels
ranged from 2.0 to 66.0 yg/dl. The median blood lead for the entire U.S. population is 13.0
pg/dl. It is readily apparent that blacks have a higher blood lead level than whites (medians
for blacks and whites were 15,0 and 13.0 respectively).
Tables 11-2 through 11-4 display the observed distribution of measured blood lead levels
by race, sex and age. The possible influence of measurement error on the percent distribution
estimates is discussed in Section 11,3.5. Estimates of mean blood lead levels differ sub-
stantially with respect to age, race and sex. Blacks have higher levels than whites, the
PB11A2/B 11-11 7/29/83
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PRELIMINARY DRAFT
TABU 11-2. HHANES II BLOOD LEAD «VELS OF PERSONS 6 MONTHS-74 YEARS, WITH WEIGHTED ARITHMETIC MEAN, STANOARO ERROR OF THE
REAM, WEIGHTED GEOMETRIC MEAN, MEDIAN, AND PERCENT DISTRIBUTION, BY RACE AND AGE, UNITED STATES, 1976-80
Blood lead level (nfl/dl)
Estimated
population Arith- Standard
in Nuaber . aetic error of
Race and age thousands exaained Mean the man
All races6
All ages 203,554 9,933 13.9 0.24
6 Mnths-S years .... 16,852 2,372 16.0 0.42
6-17 years 44,964 1,720 12.5 0.30
18-74 years 141,728 5,841 14.2 0.25
White
All ages 174,528 8,369 13.7 0.24
6 aonths-5 years . . . . 13,641 1,876 14.9 0.43
6-17 years 37,530 1,424 12.1 0.30
18-74 years 123,357 5,069 14,1 0.25
Black
All ages . . 23,853 1,332 15.7 0.48
6 aonths-5 years .... 2,584 419 20.9 0.61
6-17 years 6,529 263 14.8 0.53
18-74 years 14,740 650 15.5 0.54
aAt the Midpoint of the survey, March 1, 1978.
*\fitli lead determinations from blood specimens drawn by venipuncture.
cIncludes date for races not shown separately.
dNumbers aay not add to 100 percent due to rounding.
Geometric
Mean
Median
less
than
10
10-19 20-29 30-39
40*
Percent distribution
12.8
14.9
11.7
13.1
12.6
14.0
11.3
12.9
14.6
19.6
14.0
14.4
13.0
15.0
12.0
13.0
13.0
14.0
11.0
13.0
15.0
20.0
14.0
14,0
22.1
12.2
27.6
21.2
23.3
14.5
30.4
21.9
13.3
2.5
12.8
14.7
62.9
63.3
64.8
62.3
62.8
67.5
63.4
62.3
63.7
45.4
70.9
62.9
13.0
20.5
7.1
14.3
12.2
16.1
5.8
13.7
20.0
39.9
15.6
19.6
1.6
3.6
0.5
1.8
1.5
1.8
0.4
1.8
2.3
10.2
0.7
2.0
0.3
0.4
0.4
0.3
0.2
0.4
0.6
2.0
0.9
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PRELIMINARY DRAFT
TABLE 11-3. HHANCS II BLOOD LEAD LEVELS OF HALES 6 MONTHS-74 YEARS. KITH WEIGHTED ARITHMETIC MEAN, STANDARD ERRCR OF THE
MtAN*JftIGHTEO GEOMETRIC MEAN, MEDIAN, AND PERCENT DISTRIBUTION, BY RACE AND AGE, UNITED SIATES, 19/5-80
Blood lead level (pqAil)
Race and age
EstiMled
population
: in a
thousands
Nuater .
exaaitted
Arith-
metic
Mean
Standard
error of
the aean
Geometric
Mean
Median
Less
than
10
10-19
20-29
30-39
40*
All races'*
Percent distribution^
All ages
99,062
4,945
16.1
0.26
15.0
15.0
10.4
65.4
20.8
2.8
0.5
6 aonths-5 years . . . .
8,621
1,247
16.3
0.46
15.1
15.0
11.0
63.5
21.2
4.0
0.3
6-17 years
22,887
902
13.6
0.32
12.8
13.0
19.1
70.1
10.2
0.7
-
18-74 years
67,555
2,796
16.8
0.28
15.8
16.0
7.6
64.1
24.2
3.4
0.6
White
All ages
85,112
4,153
15.8
0.27
14.7
15.0
11.3
66.0
19.6
2.6
0.4
6 «wftths-5 years . . , .
6,910
969
15.2
0.46
14.2
14.0
13.0
67.6
17.3
2.0
0.1
6-17 years
19,060
753
13.1
0.33
12.4
13.0
21.4
69.5
8.4
0.7
-
18-74 years.
59,142
2,431
16.6
0.29
15.6
16.0
8.1
64.8
23.3
3.3
0.6
Black
All ages
11,171
664
18.3
0.52
17.3
17.0
4.0
59.6
31.0
4.1
1.3
6 wonths-5 years . . . .
1,307
231
20.7
0.74
19.3
19.0
2.7
48.8
35.1
ii. i
2.4
6-17 years
3,272
129
16.0
0.62
15.3
15.0
8.0
69.9
21.1
1.0
-
18-74 years
6,592
304
19.1
0.70
18.1
18.0
2.3
56.4
34.9
*•5
1.8
*At the Midpoint of the survey, March 1, 1978.
^ith lead deter*inations froa blood specimens drawn by venipuncture.
cIncludes date.for races not shown separately.
dNu«bers aay not add to 100 percent due to rounding.
t.
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PRELIMINARY ORAM
TABLE 11-4. NHANES II BLOOD LEAD LEVELS OF FEMALES 6 MONTHS-74 YEARS, WITH WEIGHTED ARITHMETIC MEAN,
STANDARD ERROR OF THE MEAN, WEIGHTED GEOMETRIC MEAN, MEDIAN, AND PERCENT DISTRIBUTION, BY RACE AND AGE, UNITED STATES, 1976-80
Blood lead level (pg/dl)
Race and age
Estimated
population
a
thousands
Number *
examined^
Arith-
metic
Mean
Standard
error of
the mean
Geometric
Mean Median
Less
than
10
10-19
20-29
30-39
40+
AH races®
Percent distribution'1
All ages
104,492
4,MS
11.9
0.23
11.1
11.0
33.3
60.5
5.7
0.4
0.2
6 months-5 years ....
8,241
1,125
15.8
0.42
14.6
15.0
13.5
63.2
19.8
3.0
0.5
6-17 years
22,077
818
11.4
0.32
10.6
11.0
36.6
59.3
3.9
0.2
-
18-74 years
74,173
3,045
11.8
0.22
11.0
11.0
33.7
6p.S
5.2
0.3
0.2
White
All ages
89,417
4,216
11.7
0.23
10.9
11.0
34.8
59.6
5.0
0.4
0.2
6 Months-5 years ....
6,732
907
14.7
0.44
13.7
14.0
16.1
67.3
14.8
1.6
0.2
6-17 years
18,470
671
11.0
0.31
10.3
11.0
40.0
56.9
2.9
0.2
-
18-74 years
64,215
2,638
11.7
0.23
10.9
11.0
34.6
59.9
5.0
0.4
0.2
Black
Alt ages
12,682
668
13.4
0.45
12.6
13.0
21.5
67.3
10.3
0.7
0.1
6 months-5 years ....
1,277
188
21.0
0.69
19.8
20.0
2.2
41.6
45.3
9.2
1.7
6-17 years
3,256
134
13.6
0.64
12.8
13.0
17.7
71.9
10.0
0.4
-
18-74 years
8,148
346
12.7
0.44
12.0
12.0
24.7
68.1
7.2
-
-
*At the Midpoint of the survey, March 1, 1978,
bWith lead determinations from blood specimens drawn by venipuncture.
cIncludes date for races not shown separately.
^Numbers May not add to 100 percent due to rounding.
-------
PRELIMINARY DRAFT
6-month to 5-year group is higher than the older age groups, and men are higher than women.
Overall, younger children show only a slight age effect, with 2- to 3-year-olds having slight-
ly higher blood lead levels than older children or adults (see Figure 11-3). In the 6-17 year
grouping there is a decreasing trend in lead levels with increasing age. Holding age constant,
there are significant race and sex differences; as age increases, the difference in mean blood
leads between males and females increases.
For adults 18-74 years, males have greater blood lead levels than females for both whites
and blacks. There is a significant relationship between age and blood lead, but it differs
for whites and blacks. Whites display increasing blood lead levels until 35-44 years of age
and then a decline, while blacks have increasing blood lead levels until 55-64.
This study showed a clear relationship between blood lead level and family income group.
For both blacks and whites, increasing family income is associated with lower blood lead level.
At the highest income level the difference between blacks and whites is the smallest, although
blacks still have significantly higher blood lead levels than whites. The racial difference
was greatest for the 6-month to 5-year age range.
The NHANES II blood lead data were also examined with respect to the degree of urbaniza-
tion at the place of residence. The three categories used were urban areas with population
greater than one million, urban areas with population less than one million and rural areas.
Geometric mean blood lead levels increased with degree of urbanization for all race-age groups
except for blacks 18-74 years of age (see Table 11-5). Most importantly, urban black children
aged 6 months to 5 years appeared to have distinctly higher mean blood lead levels than any
other population subgroup.
11.3.3.2 The Childhood Blood Lead Screening Programs. In addition to the nationwide picture
presented by the NHANES II (Annest et al., 1982) study regarding important demographic corre-
lates of blood lead levels, Billlck et al. (1979, 1982) provide large scale analyses of blood
lead values in specific cities that also address this issue.,
Billick et al. (1979) analyzed data from New York City blood lead screening programs from
1970 through 1976. The data include age in months, sex, race, residence expressed as health
district, screening information and blood lead values expressed in intervals of 10 mg/dl.
Only the venous blood lead data (178,588 values), clearly Identified as coming from the first
screening of a given child, were used. All blood lead determinations were done by the same
laboratory. Table 11-6 presents the geometric means of the children's blood lead levels by
age, race and year of collection. The annual means were calculated from the four quarterly
means which were estimated by the method of Hasselblad et al. (1980).
PB11A2/B
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PRELIMINARY DRAFT
AGE, years
Figure 11-3. Geometric mean blood lead levels by race and age for younger children in
the NHANES II study. The data were furnished by the National Center of Health
Statistics.
PB11A2/B
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PRELIMINARY DRAFT
TABLE 11-5. WEIGHTED GEOMETRIC MEAN BLOOD LEAD LEVELS
FROM NHANES II SURVEY BY DEGREE OF URBANIZATION OF PLACE OF
RESIDENCE IN THE U.S. BY AGE AND RACE, UNITED STATES 1976-80
Degree of urbanization
Race and age
Urban,
51 million
Urban,
<1 million
Rural
All races
Geometric
mean ((jg/dl)
All ages
14.0
(2,395)a
12.8
(3,869)
11.9
(3,669)
6 months-5 years
16.8
(544)
15.3
(944)
13.1
(884)
6-17 years
13.1
(414)
11.7
(638)
10.7
(668)
18-74 years
14.1
(1,437)
12.9
(2,287)
12.2
(2,117)
Whites
All ages
14.0
(1,767)
12.5
(3,144)
11.7
(3,458)
6 months-5 years
15.6
(358)
14.4
(699)
12.7
(819)
6-17 years
12.7
(294)
11.4
(510)
10.5
(620)
18-74 years
14.3
(1,115)
12.7
(1,935)
12.1
(2,019)
Blacks
All ages
14.4
(570)
14.7
(612)
14.4
(150)
6 months-5 years
20.9
(172)
19.3
(205)
16.4
(42)
6-17 years
14.6
(111)
13.6
(113)
12.9
(39)
18-74 years
13.9
(287)
14.7
(294)
14.9
(69)
aNumber with lead determinations from blood specimens drawn by venipuncture.
Source: Annest et al., 1982.
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TABLE 11-6, ANNUAL GEOMETRIC MEAN BLOOD LEAD LEVELS FROM THE NEW YORK BLOOD LEAD SCREENING STUDIES
OF BILLICK ET AL. (1979). ANNUAL GEOMETRIC MEANS ARE CALCULATED FROM QUARTERLY
GEOMETRIC MEANS ESTIMATED BY THE METHOD OF HASSELBLAD ET AL. (1980)
Geometric mean blood lead level, ng/100 ml
Ethnic group
Year
1-12 mo
13-24 ma
25-36 mo
37-48 mo
49-60 no
61-72 mo
73- mo
All ages
Black
1970
25.2
28.9
30.1
28.3
27.8
26.4
25.9
27.5
1971
24.0
29.3
29.9
29.3
28.2
27.2
26.5
27.7
1972
22.2
26.0
26.3
25.4
24.7
23.9
23.3
24.5
1973
22.9
26.6
26.0
25.3
24.4
24.1
23.3
24.6
1974
22.0
25.5
25.4
24.3
23.4
21.8
21.9
23.4
1975
19.8
22.4
22.4
21.9
21.2
21.4
18.9
21.1
1976
16.9
20.0
20.6
20.2
19.5
18.2
18.4
19.1
Hispanic
1970
20.8
23.8
24.5
24.7
23.8
23.6
23.0
23.4
1971
19.9
22.6
24.6
24.4
23.9
23.4
23.5
23.1
1972
18.7
20.5
21.8
22.2
21.8
21.8
21.0
21.1
. 1973
20.2
21.8
22.5
22.8
22.0
21.5
21.7
21.8
1974
19.8
21.5
22.7
22.5
21.9
20.5
20.2
21.3
1975
16.3
18.7
19.9
20.1
19.8
19.2
17.2
18.7
1976
16.0
17.4
18.1
18.2
18.0
16.7
17.2
17.4
White
1970
21.1
25.2
26.0
24.8
26.0
22.6
21.3
23.8
1971
22.5
22.7
22.7
23.5
21.6
21.3
19.5
21.9
1972
20.1
21.6
20.7
20.8
21.0
20.2
17.3
20.2
1973
21.5
21.8
21.7
20.2
21.3
20.7
18.4
20.8
1974
20.4
21.7
21.3
21.1
20.6
19.5
17.3
20.2
1975
19.3
17.9
16.1
18.5
16.8
15.4
15.9
17.1
1976
15.2
18.2
17.1
16.6
16.2
15.9
8.8
15.1
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PRELIMINARY DRAFT
All racial/ethnic groups show an increase in geometric mean blood level with age for the
first two years and a general decrease in the" older age groups. Figure 11-4 shows the trends
for all years (1970-1976) combined.
The childhood screening data described by Billick et al. (1979) show higher geometric
mean blood lead values for blacks than for Hispanics or for whites. Table 11-6 also presents
these geometric means for the three racial/ethnic groups for seven years. Using the method of
Hasselblad et al. (1980), the estimated geometric standard deviations were 1.41, 1.42 and 1.42
for blacks, Hispanics and whites, respectively.
11.3.4 Time Trends
In the past few years a number of reports have appeared that examined trends in blood
lead levels during the 1970's. In several of these reports some environmental exposure esti-
mates are available.
11.3.4.1 Time Trends in the Childhood lead Poisoning Screening Programs. Billick and col-
mmmmm—M»—p— I 111 ipn^ww—mmmmmmmmmmmmmttrn—
leagues have analyzed the results of blood lead screening programs conducted by the City of
New York (Billick et al., 1979; Billick 1982). Most details regarding this data set were al-
ready described, but Table 11-7 summarizes relevant methodologic information for these
analyses and for analyses done on a similar data base from Chicago, Illinois. The discussion
of the New York data below is limited to an exposition of the time trend in blood lead levels
from 1970 to 1977.
Geometric mean blood lead levels decreased for all three racial groups and for almost all
age groups in the period 1970-76 (Table 11-6). Table 11-8 shows that the downward trend
covers the entire range of the frequency distribution of blood lead levels. The decline in
blood lead levels showed seasonal variability, but the decrease in time was consistent for
each season. The 1977 data were supplied to EPA by Dr. Billick.
In addition to this time trend observed in New York City, Billick (1982) examined similar
data from Chicago and Louisville. The Chicago data set was much more complete than the Louis-
ville one, and was much more methodologically consistent. Therefore, only the Chicago data
will be discussed here. The lead poisoning screening program in Chicago may be the longest
continuous program in the United States. Data used in this report covered the years 1967-1980.
Because the data set was so large, only a 1 in 30 sample of laboratory records was coded for
statistical analysis (similar to procetiOVWH/ited for New York described above).
The blood lead data for Chicago contains samples that may be repeats, confirmatory analy-
ses, or even samples collected during treatment, as well as initial screening samples. This
is a major difference from the New York City data, which had initial screening values only.
PB11A2/B
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PRELIMINARY DRAFT
30
25 —
S
3
2*
ut
20
16
O
o
3
so
2
m 10
~ Slacks
O Whites
A Hispanic#
AGE, years
Figure 11-4. Geometric mean blood toad values by race and age for younger children
in the New York City screening program (1970-1976).
PB11A2/8
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PRELIMINARY DRAFT
TABLE 11-7. CHARACTERISTICS OF CHILDHOOD LEAD POISONING SCREENING DATA
New York
Chicago
Time period
1970 - 1979
1967 - 1980 (QTR 2)
Sampling technique
Venous
Venous
Analytic technique
AAS
(Hasel method)
AAS
(Hasel method)
Laboratory
In house
In house
Screening status
Available/unknown
Unavailable
Race classification
and total number of
samples used in
analysis*
Unknown 69,658
White 5,922
Black 51,210
Hispanic 41,364
Other 4,398
TOTAL 172,552
Nonblack 6,459
Black 20,353
TOTAL 26,812
Raw data
Decade grouped
Ungrouped
Gasoline data
Tri-state (NY, NJ, CT)
1970 - 1979
SMSA 1974 - 1979
SMSA
'"New York data set only includes first screens while Chicago includes also
confirmatory and repeat samples.
TABLE 11-8. DISTRIBUTION OF BLOOD LEAD LEVELS FOR 13 TO 48
MONTH OLD BLACKS BY SEASON AND YEAR* FOR NEW YORK SCREENING DATA
January - Marih
July - September
Percent
Percent
Year
<15pg/dl
15 to 34pg/dl
>34|jg/dl
<15Mg/dl
15 to 34pg/dl
>34pg/dl
1970
(insufficient sample size)
3.4
54.7
42.0
1971
3.8
69.5
26.7
1.3
56.0
42.7
1972
4.4
76.1
19.5
4.3
72.2
23.4
1973
7.3
80.3
12.4
2.7
62.4
34.9
1974
9.2
73.8
17.0
8.2
65.4
26.4
1975
11.1**
77.5**
11.4**
7.3**
81.3**
11.4**
1976
21.1
74.1
4.8
11.9
75.8
12.3
1977
28.4
66.8
4.8
19.9
72.9
7.2
* data provided by I.H. Billick
**Percents estimated using interpolation assuming a lognormal distribution.
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PRELIMINARY DRAFT
Chicago blood lead levels were all obtained on venous samples and were analyzed by one labora-
tory, the Division of Laboratories, Chicago Department of Health. Lead determinations were
done by atomic absorption. Racial composition was described in more detail than for New York,
but analysis showed there was no difference among the non-blacks, so they were pooled in the
final analysis.
Table 11-7 displays important characteristics of the Chicago and New York screening pro-
grams, including the number of observations involved in these studies. From tables in the ap-
pendices of the report (Billick, 1982), specific data on geometric mean blood lead values,
race, sex and sampling data for both cities are available. Consistency of the data across
cities is depicted in Figure 11-5. The long-term trends are quite consistent, although the
seasonal peaks are somewhat less apparent.
11.3.4.2 Newark. Gause et al. (1977) present data from Newark, New Jersey, that reinforce
the findings of Billick and coworkers. Gause et al. studied the levels of blood lead among 5-
and 6-year-old children tested by the Newark Board of Education during the academic years
1973-74, 1974-75 and 1975-76. All Newark schools participated in all years. Participation
rates were 34, 33 and 37 percent of the eligible children for the three years, respectively.
Blood samples were collected by fingerstlck onto filter paper. The samples were then
analyzed for lead by atomic absorption spectrophotometry. The authors point out that finger-
stick samples are more subject to contamination than venous samples; and that because erythro-
cyte protoporphyrin confirmation of blood lead values greater than 50 Mfl/dl was not done until
1974, data from earlier years may contain somewhat higher proportions of false positives than
.later years.
Blood lead levels declined markedly during this 3-year period. In the three years covered
by the study the percentage of children with blood lead levels less than 30 yg/dl went from 42
percent for blacks in 1973-74 to 71 percent -in 1975-76; similarly, the percentages went from
56 percent to 85 percent in whites. The percentage of high risk children (>49 pg/dl) dropped
from 9 to 1 percent in blacks and from 6 to 1 percent in whites during the study period.
Unfortunately, no companion analysis was presented regarding concurrent trends in en-
vironmental exposures. However, Foster et al. (1979) reported a study from Newark that exam-
ined the effectiveness of the city's housing deleaving program, using the current blood lead
status of children who had earlier been idefltMngtf^ss having confirmed elevated blood lead
levels; according to the deleadlng program, these children's homes should have been treated to
alleviate the lead problem. After intensive examination, the investigators found that 31 of
the 100 children studied had lead-related symptoms at the time of Foster's study. Examination
of the records of the program regarding the deleading activity indicated a serious lack of
compliance with the program requirements. Given the results of Foster's study, it seems un-
likely that the observed trend was caused by the deleading program.
PB11A2/B 11-22 7/29/83
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PRELIMINARY DRAFT
SO
t—i—n—i—i—rr
i
8
40 —
CHICAGO
NEW VORK
10
1870 1971 1972 1973 1974 1976 1979 1977 1978 1879 1980
YEAR (Beginning Jan. 1)
Figure 11-5. Time dependence of blood lead for blacks, aged 24 to 35
months. In New York City and Chicago.
Source: Adapted from BHHck (1982).
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11.3.4.3 Boston. Rabinowitz and Needleman (1982) report a study of umbilical cord blood lead
levels from 11,837 births between April 1979 and April 1981 in the Boston area. These repre-
sent 97 percent of the births occurring in a hospital serving a diverse population. Blood
samples were analyzed for lead by anodic stripping voltammetry after stringent quality control
procedures were used. External quality control checks were done by participation in the Blood
Lead Reference Program, conducted by the Centers for Disease Control. The average difference
between the investigators' results and the reference lab was 1.4 pg/dl.
The overall mean blood lead concentration was 6.56 ± 3,19 (standard deviation) with a
range from 0.0 to 37.0 pg/dl. A downward trend in umbilical cord blood lead levels (-0.89
pg/dl/yr) was noted over the two years of the study (see Figure 11-6).
11.3.4.4 NHANES II. Blood lead data from NHANES II (see Section 11.3.3.1) also show a signi-
ficant downward trend over time (Annest et al., 1983). Predicted mean blood lead levels
dropped from 14.6 Mfl/dl in February 1976 to 9.2 pg/dl in February of 1980. Mean values from
these national data presented in 28 day intervals from February 1976 to February 1980 are dis-
played in Figure 11-7.
The decreases in average blood lead levels were found for both blacks and whites, all age
groups and both sexes. Further statistical analysis suggested that the decline was not en-
tirely due to season, income, geographic region or urban-rural differences. The analyses of
the quality control data showed no trend in the blind quality control data.
A review panel has examined this data, and a report of their findings is in Appendix 11-0.
The panel concluded that there was strong evidence of a downward trend during the period of
the study. The panel further stated that the magnitude of this drop could be estimated, and
that it appeared not only in the entire population, but in some major subgroups as well.
11.3.4.5 Other Studies. Oxley (1982) reported an English study that looks at the recent past
time trend in blood lead levels. Preemployment physicals conducted in 1967-69 and 1978-80
provided the subjects for the study. Blood samples were collected by venipuncture. Different
analytical procedures were used in the two surveys, but a comparison study showed that the
data from one procedure could be reliably adjusted to the other procedure. The geometric mean
blood lead levels declined from 20.2 to 16.6 yg/dl.
11.3.5 Distributional Aspects of Population Blood lead Levels
The importance of the distribution form of blood lead levels was briefly discussed in
Section 11.2.3. The distribution form determines which measure of central tendency (arith-
metic mean, geometric mean, median) is most appropriate. It is even more important in esti-
mating percentiles in the upper tail of the distribution, an issue of much importance in esti-
mating percentages (or absolute numbers) of individuals in specific population groups likely
to be experiencing various lead exposure levels.
PB11A2/B 11-24 7/29/83
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PRELIMINARY DRAFT
12.0
(.0
•V;
Modal Predicted
4.0
• Actual Data
1/80
4/ao
10/80
TIME, days
Figure 11-6. Modeled umbilical cord blood lead levels by date of sample collection
for infants in Boston.
Source; Rabinowitz and Needleman (1982).
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WINTER 1976
(FEB.)
WINTER 1977
(FEB.)
WINTER 1978
(FEB.)
FALL 1978 WINTER 1979
(OCT.)
WINTER 1900
(FEB.)
FEB.)
0
6
10
50
16
20
25
30
36
40
46
66
CHRONOLOGICAL ORDER, 1 unit = 28 days
Figure 11-7. Average blood lead levels of U.S. population 6 months—74 years. United States,
February 1976—February 1980, based on dates of examination of NHANES II examinees with
blood lead determinations.
Source: Annest et al. (1983).
-------
PRELIMINARY DRAFT
Distribution fitting requires large numbers of samples taken from a relatively homo-
geneous population. A homogeneous population is one in which the distribution of values
remains constant when split into subpopulations. These subpopulations could be defined by
demographic factors such as race, age, sex, income, degree of urbanization, and by degree of
exposure. Since these factors always have some effect, a relatively homogeneous population
will be defined as one with minimal effects from any factors that contribute to differences in
blood lead levels.
Several authors have suggested that the distribution of blood lead levels for any rela-
tively homogeneous population closely follows a lognormal distribution (Yankel et al., 1977;
Tepper and Levin, 1975; Azar et al., 1975). Lognormality has been noted for other metals,
such as 90Sr, 144Ce, Pu and Ti in various tissues of human populations (Cuddihy et al., 1979;
Schubert et al., 1967). Yankel et al. (1977), Tepper and Levin (3^75) and Angle and Hclntire
(1979) all found their blood lead data to be lognormally distributed. Further analysis by EPA
of the Houston study of Johnson et al. (1974), the study of Azar et al. (1975) and the New
York children screening program reported by Billick et al. (1979) also demonstrated that a
lognormal distribution provided a good fit to the data.
The only nationwide survey of blood lead levels in the U.S. population is the NHANES II
survey (Annest et al., 1982). In order to obtain a relatively homogeneous subpopulation of
lower environmental exposure, the analysis was restricted to whites not living in an SMSA with
a family income greater than $6,000 per year, the poverty threshold for a family of four at
the midpoint of study as determined by the U.S. Bureau of Census. This subpopulation was
split into four subgroups based on age and sex. The summary statistics for these subgroups
are in Table 11-9.
Each of these four subpopulations were fitted to five different distributions: normal,
lognormal, gamma, Weibull and Wald (Inverse Gaussian) as shown in Table 11-10. Standard chi-
square goodness-of-fit tests were computed after collapsing the tails to obtain an expected
cell size of five. The goodness-of-fit test and likelihood functions indicate that the log-
normal distribution provides a better fit than the normal, gamma or Weibull. A histogram and
the lognormal fit for each of the four subpopulations appear in Figure 11-8. The Wald distri-
bution is quite similar to the lognormal distribution and appears to provide almost as good a
fit. Table 11-10 also Indicates that the lognormal distribution estimates the 99th percentile
as well as any other distribution.
Based on the examination of the NHANES II data, as well as the results of several other
papers, it appears that the lognormal distribution is the most appropriate for describing the
distribution blood lead levels in homogeneous populations with relatively constant exposure
levels.
PB11A2/B
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PRELIMINARY DRAFT
The lognormal distribution appears to fit well across the entire range of the distribution,
including the right tail. It should be noted, however, that the data being fitted are the
result of both measurement variation and population variation. The measurement variation
alone does not follow a lognormal distribution, as was shown by Saltzman et al., 1983.
TABLE 11-9. SUMMARY OF UNWEIGHTED BLOOD LEAD LEVELS IN WHITES
NOT LIVING IN AN SMSA WITH FAMILY INCOME GREATER THAN $6,000
Unweighted Mean
Sample
Arith.
Geom.
Sample
99th
Arith.
Geom.
Subgroup
Size
Mean
Mean
Median
Xtile
Std. Dev.
Std. Dev.
pg/dl
Mg/dl
Mg/dl
Mg/dl
Mg/di
M8/dl
age 1/2 to 6
752
13.7
12.9
13.0
32.0
5.03
1.43
age 6 to 18
573
11.3
10.6
10.0
24.0
4.34
1.46
age 18+,men
922
15.7
14.7
15.0
35.8
5.95
1.44
age 18+,women
927
10.7
10.0
10.0
23.0
4.14
1.46
It 1s obvious that even relatively homogeneous populations have considerable variation
among individuals. The estimation of this variation is Important for determination of the
upper tail of the blood lead distribution, the group at highest risk. The NHANES *11 study
provides sufficent data to estimate this variation. In order to minimize the effects of loca-
tion, income, sex and age, an analysis of variance procedure was used to estimate the varia-
tion for several age-race groups. The variables just mentioned were used as main effects, and
the resulting mean square errors of the logarithms are in Table 11-11. The estimated
geometric standard deviations represent the estimated variances for subgroups with comparable
sex, age, income and place of residence. These are not necessarily representative of the
variances seen for specific subgroups described in the NHANES II study.
Analytical variation, which exists in any measurement of any kind, has an impact on the
bias and precision of statistical estimates. For this reason, it is Important to estimate the
magnitude of variation. Analytical variation consists of both measurement variation (vari-
ation between measurements run at the same time) and variation created by analyzing samples at
different times (days). This kind of variation for blood lead determinations has been dis-
cussed by Lucas (1981).
The NHANES II survey is an example of a study with excellent quality control data. The
analytical variation was estimated specifically for this study by Annest et al. (1983). The
analytical variation was estimated as the sum of components estimated from the high and low
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TABLE 11-10. SUMMARY OF FITS TO NHANES II BLOOD LEAD LEVELS
OF WHITES NOT LIVING IN AN SMSA, INCOME GREATER THAN $6,000,
FOR FIVE DIFFERENT TWO-PARAMETER DISTRIBUTIONS
Children <6 years
deviation*
log-
at
Chi-square
D.F.
p-value
likelihood
99 Xtile
Normal
75.52
8
0.0000
-2280.32
6.61
Lognormal
14.75
10
0.1416
-2210.50
2.57
Gamma
17.51
9
0.0413
-2216.51
4.68
Weibull
66.77
8
0.0000
-2271.57
5.51
Wald
15.71
10
0.1083
-2211.83
2.76
Children 6S years £17
deviation*
log-
at
Chi-square
D.F.
p-value
likelihood
99 Xtile
Normal
39.58
6
0.0000
-1653.92
2.58
Lognormal
3.22
8
0.9197
-1607.70
-1.50
Gamma
4.88
7
0.6745
-1609.33
-0.64
Weibull
24.48
6
0.0004
-1641.35
1.72
Wald
2
8
0.9480
-1609.64
-1.30
Men 618 years
deviation*
log-
at
Chi-square
D.F.
p-value
likelihood
99 Xtile
Normal
156.98
10
0.0000
-2952.85
6.24
Lognormal
12.22
13
0.5098
-2854.04
1.51
Gamma
34.26
12
0.0006
-2864.79
4.00
Weibull
132.91
11
0.0000
-2934.14
4.88
Wald
14.42
13
0.3450
-2855.94
1.72
Men 218 years
deviation*
log-
at
Chi-square
D.F.
p-value
likelihood
99 Xtile
Normal
66.31
5
0.0000
-2631.67
2.68
Lognormal
7.70
8
0.4632
-2552.12
-1.18
Gamma
11.28
7
0.1267
-2553.34
0.90
Weibull
56.70
6
0.0000
-2611.78
1.73
Wald
10.26
8
0.2469
-2556.88
-1.01
•observed 99th sample percentile minus predicted 99th percentile
PB11A2/B 11-29 7/29/83
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PRELIMINARY DRAFT
>
u
z
~
o
z
LU
3
2
i
tti
3
a
Ul
i
o
23.5
31.6
31.6
7.6
16.6
7.6
16.6
23.6
0
BLOOD LEAD LEVELS {fig/dll BLOOD LEAD LEVELS (^dl)
FOR 6 MONTHS TO 6 YEAR OLD CHILDREN FOR 6 TO 17 YEAR OLD CHILDREN
7.S
16.6
23.6
31.6
7J
16.6
23.6 31.6
BLOOD LEAD LEVELS Wdll
FOR MEN >18 YEARS OLD
BLOOD LEAD LEVELS (wj/dl)
FOR WOMEN >18 YEARS OLD
Figure 11-8. Histograms of blood lead levels with fitted lognormal curves for the NHAN1S II
study. All subgroups are white, non-SMSA residents with family incomes greater titan 16000.
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TABLE 11-11. ESTIMATED MEAN SQUARE ERRORS RESULTING FROM
ANALYSIS OF VARIANCE ON VARIOUS SUBPOPULATIQNS
OF THE NHANES II DATA USING UNWEIGHTED DATA
Age
White,
Non SMSA
White, SMSA,
not central city
White,
central city
Slack,
central city
0,5 to 6
0.0916
0.0839
0.1074
. 0.0978
(1.35)*
(1.34)
(1.39)
(1.37)
6 to 18
0.0814
0.0724
0.0790
0.0691
(1.33)
(1.31)
(1.33)
(1.30)
18+, men
0.1155
0.0979
0.1127
0.1125
(1.40)
(1.37)
(1.40)
|
(1-40)
18+, women
0.1083
0.0977
0.0915
0.0824
(1.39)
(1.37)
(1.35)
(1.33)
Note: Mean square errors are based on the logarithm of the blood lead levels.
•Estimated geometric standard deviations are given In parentheses.
blind pool and from the replicate measurements 1n the study of Griffin et al. (1975). The
overall estimate of analytical variation for the NHANES II study was 0.02083.
Analytical variation causes a certain amount of misclasslflcation when estimates of the
percent of Individuals above or below a given threshold are made. This is because the true
value of a person's blood lead could be below the threshold, but the contribution from analy-
tical variation may push the observed value over the threshold. The reverse is also possible.
These two types of misclassifications do not necessarily balance each other.
Annest et al. (1983) estimated this misclassiflcation rate for several subpopulations In
the NHANES II data using a threshold value of 30 yg/dl. In general, the percent truly greater
than this threshold yas approximately 24 percent less than the prevalence of blood lead levels
equal to or greater than 30 Mg/dl, estimated from the weighted NHANES II data. This 1s less
than the values predicted by Lucas (1981) which were based on some earlier studies.
11.3.6 Exposure Covarlates of Blood Lead Levels In Urban Children
Results obtained from the NHANES II study show that urban children generally have the
highest blood lead levels of any non-occupationally exposed population group. Furthermore,
black urban children have significantly higher blood lead levels than white urban children.
Several studies have been reported in the past few years that look at determinants of blood
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lead levels in urban children (Stark et at., 1982; Charney et al., 1980; Hammond et al., 1980;
Gilbert et al., 1979).
11.3.6.1 Stark Study. Stark et al, (1982) used a large scale lead screening program in New
Haven, Connecticut, during 1974-77 as a means of identifying study subjects. The screening
program had blood lead levels on 8289 children ages 1-72 months, that represented about 80
percent of the total city population 1n that age group. From this initial population, a much
smaller subset of children was identified for a detailed environmental exposure study. Using
the classifying criteria of residential stability and repeatable blood lead levels (multiple
Measurements fell into one of three previously defined blood lead concentration categories), a
potential study population of 784 was identified. Change of residence following identifica-
tion and refusal to let sanitarians make inspections resulted in 407 children being dropped;
the final study population contained 377 children.
With the exception of dietary lead intake, each child's potential total lead exposure was
assessed. Information was obtained on lead in air, house dust, interior and exterior paint
and soil near and far from the home. A two percent sample of homes with children having
elevated lead levels had tap water lead levels assessed. No water lead levels above the
public health service standard of 50 pg/1 were found. Socioeconomic variables were also
obtained.
For all children in the study, micro blood samples were taken and analyzed for lead by
AAS with Delves cup attachment. Blood lead values were found to fellow a lognormal distri-
bution. Study results were presented using geometric means and geometric standard deviation.
Among the various environmental measurements a number of significant correlation coefficients
were observed. However, air lead levels were independent of most of the other environmental
variables. Environmental levels of lead did not directly follow socioeconomic status. Most
of the children, however, were in the lower socioeconomic groups.
Multiple regression analyses were performed by Stark et al. (1982) and by EPA*. Stark
and coworkers derived a log-log model with R2 = 0.11, and no significant effects of race or
age were found. EPA fitted a linear exposure model 1n logarithmic form with results shown in
Table 11-12. Significant differences among age groups were noted, with considerably improved
predictability (R2 = 0.29, 0.30, 0.14 for ages 0-1, 2-3, and 4-7). Sex was not a significant
variable, but race equal black was significant at ages 4-7. Air lead did not significantly
improve the fit of the model when other covariates were available, particularly dust, soil,
paint and housekeeping quality. However, the range of air lead levels was small (0.7-1.3
pg/ms) and some of the inhalation effect may have been confounded with dust and soil inges-
tion. Seasonal variations were important at all ages.
*N0TE: The term EPA analyses refers to calculations done at EPA. A brief discussion of the
methods used is contained in Appendix 11-8; more detailed information 1s available at EPA
upon request.
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TABLE 11-12. MULTIPLE REGRESSION MODELS FOR BLOOD LEAD
OF CHILDREN IN NEW HAVEN, CONNECTICUT,
SEPTEMBER 1974 - FEBRUARY 1977
Regression Coefficients and Standard Errors
Age group, years •0*1 2-3 4-7
Summer - Winter
6.33 ±
2.11*
3.28 t 1.30*
2.43 ± 1.38*
Dust, pg/g
0.00402 ± 0.00170*
0.00182 t 0.00066*
0.00022
± 0.00077
Housekeeping Quality
4.38 ± 2.02*
1.75 ± 1.17
-1.61 ± 1.12
Soil near house, pg/g
0.00223 ± 0.00091*
-0.00016 ± 0.00042
0.00060
± 0.00041
Soil at curb, pg/g
0.00230 1
0.00190
0.00203 ± 0.00082*
0.00073
± 0.00079
Paint, child's bedroom
0.0189 ±
0.0162
0.0312 ± 0.0066*
0.0110
± 0.0064*
Paint outside house
-0.0023 ±
0.0138
0.0200 ± 0.0069*
0.0172
± 0.0067*
Paint quality
0.89 ±
1.71
3.38 ± 0.96*
4.14
± 1.15*
Race = Black
2.16 ±
2.05
0.07 ± 1.09
5.81
± 1.00*
Residual Standard Deviations
0.1299
0.0646
0.
1052
Multiple R2
0.289
0.300
0.
143
Sample size (blood samples)
153
334
439
*Significant positive coefficient, one-tailed p <0.05
11.3.6.2 Charnev Study. Charney et al. (1980) conducted a case control study of children 1.5
to 6 years of age with highly elevated and non-elevated blood lead levels. Cases and controls
were initially identified from the lead screening programs of two Rochester, New York, health
facilities. Cases were defined as children who had at least two blood lead determinations
between 40 and 70 pg/dl and FEP values greater than 59 pg/dl during a 4-month period. Con-
trols were children who had blood lead levels equal to or less than 29 pg/dl and FEP equal to
or less than 59 pg/dl. High level children were selected first and low level children were
group matched on age, area of residence, and social class of the family. Home visits were
made to gain permission as well as to gather questionnaire and environmental data. Lead anal-
yses of the various environmental samples were done at several different laboratories. No
specification was provided regarding the analytical procedures followed.
The matching procedure worked well for age, mother's educational level and employment
status. There were more blacks in the high lead group as well as more Medicaid support. These
factors were then controlled in the analysis; no differences were noted between the high and
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low blood lead groups regarding residence on high traffic density streets (>10,000 vehicles/
day) or census tract of residence.
The two groups differed regarding mean house dust lead levels (1265 pg/sample for high
and 123 Mg/sample for low). Median values also differed, 149 vs. 55 pg/sample. One-third of
the children in the low blood lead group had house dust lead samples with more lead than those
found in any middle class home previously investigated. .
There were considerably greater quantities of lead on the hands of the high blood lead
group compared with the low group (mean values were 49 pg/sample and 21 pg/sample, respective-
ly), Hand and house dust lead levels were correlated (r =.0.25) but the relationship was not
linear. At the low end of the house dust lead values, hand dust was always low but the con-
verse was not true: not every child exposed to high house dust lead had high hand dust levels.
In addition to hand and house dust lead, other factors differentiated the high and low
blood lead groups. Although both groups had access to peeling paint in their homes (^-2/3),
paint lead concentrations exceeding 1 percent were found more frequently in the high as oppo-
sed to the low group. Pica (as defined in Chapter Seven) was more prevalent in the high lead
group as opposed to the low lead group.
Since the data suggested a multifactorial contribution of lead, a multiple regression
analysis was undertaken. The results suggest that hand lead level, house dust lead level,
lead in outside soil, and history of pica are very important in explaining the observed vari-
ance in blood lead levels.
11.3.6.3 Hammond Study. Hammond et al. (1980) conducted a study of Cincinnati children with
the dual purpose of determining whether inner city children with elevated blood lead levels
have elevated fecal lead and whether fecal lead correlates with lead-base paint hazard in the
home or traffic density as compared with blood lead.
Subjects were recruited primarily to have high blood lead levels. Some comparison chil-
dren with low blood lead levels were also Identified. The three comparison children had to be
residentially stable so that their low blood lead levels were reflective of the lead intake of
their current environment. The subjects from the inner city were usually from families in
extremely depressed socio-economic circumstances.
Stool samples were collected on a daily basis for up to 3 weeks, then analyzed for lead.
2
Fecal lead levels were expressed both as mg/kg day and as mg/m day.
An environmental assessment was made at the home of each child. Paint lead exposure was
rated on a three-point scale (high, medium and low) based on paint lead level and integrity of
the painted wall. Air lead exposure was assessed by the point scale (high, medium and low)
based on traffic density, because there are no major point sources of lead in the Cincinnati
area.
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Blood samples were collected on an irregular basis but were taken sufficiently often to
have at least one sample from a child from every house studied. The blood samples were ana-
lyzed for lead by two laboratories that had different histories of performance in the CDC pro-
ficiency testing program. All blood lead levels used in the statistical analysis were ad-
justed to a common base. Because of the variable number of fecal and blood lead levels, the
data were analyzed using a nested analysis^sf yariance.
The homes of the children were found to be distributed across the paint and traffic lead
exposure categories. Both fecal lead levels and blood lead levels were positively associated
with interior paint lead hazard, A marginal association between fecal lead levels and
exterior paint hazard was also obtained. Neither fecal lead or blood lead was found to be
associated with traffic density; the definition of the high traffic density category, however,
began at a low level of traffic flow (7500 cars/day).
Examination of fecal and blood lead levels by sex and race showed that black males had
the highest fecal lead excretion rates-fallowed by white males and black females. White fe-
males were only represented by two subjects, both of whom had high fecal lead excretion.
Blood lead levels were more influenced by race than by sex. The results suggested that chil-
dren in high and medium paint hazard homes (high = at least 1 surface >0.5 percent Pb, peeling
or loose) were probably ingesting paint in some form. This could not be confirmed, however,
by finding physical evidence in the stools.
Long term stool collection in a subset of 13 children allowed a more detailed examination
of the pattern of fecal lead excretion. Two patterns of elevated fecal lead excretion were
noted. The first was a persistent elevation compared with controls; the second was markedly
elevated occasional spikes against a normal background.
One family moved from a high hazard home to a low one during the course of the study.
This allowed a detailed examination of the speed of deleading of fecal and blood lead level.
The fecal levels decreased faster than the blood lead levels. The blood leads were still
elevated at the end of the collection.
11.3.6.4 Gilbert Study. Gilbert et al. (1979) studied a population of Hispanic youngsters in
Springfield, Massachusetts, in a case control study designed to compare the presence of
sources of lead in homes of lead poisoned children and appropriately matched controls. Cases
were defined as children having two consecutive blood lead levels greater than 50 yg/dl. Con-
trols were children with blood lead levels less than or equal to 30 Mfl/dl who had no previous
history of lead intoxication and were not siblings of children with blood lead levels greater
than 30 pg/dl. Study participants had to be residentially stable for at least 9 months and
not have moved into their current home from a lead contaminated one. All blood lead levels
were analyzed by Delves cup method of AAS. Cases and controls were matched by age (±3 months),
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sex and neighborhood area. The study population consisted of 30 lead intoxication cases and
30 control subjects.
Hone visits were undertaken to gather interview information and conduct a home in-
spection. Painted surfaces were assessed for integrity of the surface and lead content. Lead
content was measured by X-ray fluoriinetry. A surface was scored as positive if the lead con-
tent exceeded 1.2 mg/cm2. Drinking water lead was assessed for each of the cases and was
found to contain less than 50 pg/1, sufficiently low so as not to constitute a hazard. Tap
water samples were not collected in the homes of the controls. Soil samples were collected
from three sites in the yard and analyzed for lead by X-ray fluorometry.
Cases and controls were compared on environmental lead exposures and interview data using
McNemar's test for pair samples. The odds ratio was calculated as an estimator of the rela-
tive risk on all comparisons. Statistically significant differences between cases and con-
trols were noted for lead in paint and the presence of loose paint. Large odds ratios (>10)
were obtained; there appeared to be little influence of age or sex on the odds ratios.
Significant differences between cases and controls were obtained for both intact and
loose paint by individual surfaces within specific living areas of the home. Surfaces acces-
sible to children were significantly associated with lead poisoning status while Inaccessible
surfaces generally were not. Interestingly, the odds ratios tended to be larger for the in-
tact surface analysis than for the loose paint one.
Median paint lead levels in the homes of cases were substantially higher than those in
the homes of controls. The median paint lead for exterior surfaces in cases was about 16-20
mg/cm2 and about 10 mg/cm2 for interior surfaces. Control subjects lived in houses 1n which
the paint lead generally was less than 1.2 mg/cm2 except for some exterior surfaces.
Soil lead was significantly associated with lead poisoning; the median soil lead level
for homes of cases was 1430 pg/g, while the median soil lead level for control homes was
440 pg/g.
11.4 STUDIES RELATING EXTERNAL DOSE TO INTERNAL EXPOSURE
The purpose of this section is to assess the importance of environmental exposures in
determining the level of lead in human populations. Of prime interest are those studies that
yield quantitative estimates of the relationship between air lead exposures and blood lead
levels. Related to this question is the evaluation of which environmental sources of airborne
lead play a significant role in determining the overall impact of air lead exposures on blood
lead levels.
A factor that complicates the analysis presented here is that lead does not remain sus-
pended in the atmosphere but rather falls to the ground, is incorporated into soil, dust, and
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water, and enters the food chain over time (see Figure 11-1). Since man is exposed to lead
from all of these media, as will be demonstrated below, studies that relate air lead levels to
blood lead levels (especially experimental exposure studies) may underestimate the overall
impact of airborne lead on blood lead levels. In observational studies, the effects of air
lead will thus be confounded with lead exposures from other pathways. The simultaneous pre-
sence of lead in multiple environmental media requires the use of multiple variable analysis
techniques or surrogate assessment of all other external exposures. Virtually no assessments
of simultaneous exposures to all media have been done.
Although no study is ever done perfectly, there are several key factors that are present
in good studies relating external exposure to internal exposure of lead:
(1) The study population is well-defined.
(2) There is a good measure of the exposure of each individual.
(3) The response variable (blood lead) is measured with adequate quality control,
preferably with replicates.
(4) The statistical analysis model is biologically plausible and is consistent with
the data.
(5) The important covariates are either controlled for or measured.
Even studies of considerable importance do not address all of these factors adequately.
We have selected as key studies (for discussion below) those which address enough of these
factors sufficiently well to establish meaningful relationships.
11.4.1 Air Studies
The studies emphasized in this section are those most relevant to answering the following
question: If there is moderate change in average ambient air lead concentrations due to
changes in environmental exposure (at or near existing EPA air lead standards), what changes
are expected in blood lead levels of individual adults and children in the population? Longi-
tudinal studies in which changes in blood lead can be measured in single individuals as
responses to changes in air lead are discussed first. The cross-sectional relationship
between blood lead and air lead levels in an exposed population provides a useful but differ-
ent kind of information, since the population "snapshot" at some point in time does not direc-
tly measure changes in blood lead levels or responses to changes 1n air lead exposure. We
have also restricted consideration to those Individuals without known excessive occupational
or personal exposures (except, perhaps, for some children in the Kellogg/Silver Valley study).
The previously published analyses of relevant studies have not agreed on a single form
for the relationship between air lead and blood lead. All of the experimental studies have at
least partial individual air lead exposure measures, as does the cross-sectional observational
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study of Azar et al. (1975) The 1974 Kellogg/Si Iyer Valley study (Yankel et a"!., 1977) has
also been analyzed using several models. Other population cross-sectional studies have been
analyzed by Snee (1981). The most convenient method for summarizing these diverse studies and
their several analyses 1s by use of the blood lead-air lead slope (p), where p measures the
change in blood lead that is expected for a unit change in air lead. If determined for indi-
vidual subjects in a study population, this slope is denoted If the fitted equation 1s
linear, then p or p. is the slope of the straight line relationship at any air lead level. If
the fitted relationship is nonlinear, then the slope of the relationship measures the expected
effect on blood lead of a small change in air lead at some given air lead value and thus will
be somewhat different at different air lead levels. It is necessary to compare the slopes of
the nonlinear relationships at the same value of air lead or change in air lead. A discussion
of the linear, nonlinear and compartment models is in Appendix 11A-B.
Snee (1982b,c) has indicated that inclusion of additional sources of lead exposure im-
proves biological plausibility of the models. It Is desirable that these sources be as spe-
cific to site, experiment and subject as possible.
11.4.1.1 The Griffin et al. Study. In two. separate experiments conducted at the Clinton
Correctional Facility in 1971 and 1972, adult male prisoner volunteers were sequestered in a
prison hospital unit and exposed to approximately constant levels of lead oxide (average
10.9 ng/m3 in the first study and 3.2 yg/m3 in th"e second). Volunteers were exposed in an ex-
posure chamber to an artificially, generated aerosol of submicron-sized particles of lead
dioxide. All volunteers were introduced into the chamber 2 weeks before the initiation of the
exposure; the lead exposures were scheduled to last 16 weeks, although the volunteers could
drop out whenever they wished. Twenty-four volunteers, Including 6 controls, participated in
the 10.9 Mg/m3 exposure study. Not all volunteers completed the exposure regimen. Blood lead
levels were found to stabilize after approximately 12 weeks. Among 8 men exposed to 10.9
pg/m3 for at least 60 days, a stabilized mean level of 34.5 ± 5.1 pg/dl blood was obtained, as
compared with an initial level of 19.4 ±3.3 pg/dl. All but two of the 13 men exposed at 3.2
Mg/m3 for at least 60 days showed increases and an overall stabilized level of 2S.6 t 3.9
pg/dl was found, compared with an initial level of 20.5 ± 4.4 pg/dl. This represented an in-
crease of about 25 percent above the base level.
The aerosols used in this experiment were somewhat less complex chemically, as well as
somewhat smaller, than those found in the ambient environment. Griffin et al. (1975),
however, pointed out that good agreement was achieved on the basis of the comparison of their
observed blood lead levels with those predicted by Goldsmith and Hexter's (1967) equation;
that 1s, lofljo blood lead = 1.265 + 0.2433 l°g10 atmospheric air lead. The average diet con-
tent of lead was measured and blood lead levels were observed at 1- or 2-week intervals for
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several months. Eight subjects received the maximum 4-month exposure to 10.9 pg/m3; nine sub-
jects were exposed for 1 to 3 months. Six subjects had the maximum 4-month exposure to 3.2
pg/m3, and eight others had shorter exposures.
Compartmental models have been fitted to these data by 0'Flaherty et al. (1982) and by
EPA. The basis of these models is that the mass of lead in each of several distinct pools or
compartments within the body changes according to a system of coupled first-order linear dif-
ferential equations with constant fractional transfer rates (Batschelet et al., 1979; Rabino-
witz et al., 1976). Such a model predicts that when the lead intake changes from one constant
level to another, then the relationship between the mass of lead in each compartment and time
with constant intake has a single exponential term.
The subjects at 3.2 pg/m3 exhibited a smaller increase in blood lead, with corres-
pondingly less accurate estimates of the parameters. Several of the lead-exposed subjects
failed to show an increase.
Figure 11-9 shows a graph of the blood lead levels for the 10.9 pg/m3 exposure by length
of exposure. Each person's values are individually normalized, and then averaged across
100
0 10 20 30 40 EO SO 70 10 BO 100 110 120
DAY OF EXPOSURE
Figure 11-9. Graph of the average normalized increase in blood lead for subjects exposed to
10.9 fjg/m1 of lead in Griffin et al. study (1978).
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subjects for each time period. The smooth curve shows a fitted one-compartment model, assum-
ing pre-exposure equilibrium and constant lead intake during exposure.
EPA has reanalyzed these data using a two-compartment model for two reasons;
(1) Semi logarithmic plots of blood lead vs. time for most subjects showed a two-
component exponential decrease of blood lead during the postexposure or washout
phase of the experiments. Rabinowitz et al. (1977) show that at least two
pools are necessary to model blood lead kinetics accurately. The first pool is
tentatively identified with blood and the most labile soft tissues. The second
pool probably includes soft tissues and labile bone pools.
(2) Kinetic models are needed to account for the subjects' lead burdens not being
in equilibrium at any phase of the experiments.
The pre-exposure decline in Figure 11-9 is apparently real and suggests a low pre-exposure
lead intake. The deviation from the fitted curve after about 50 days suggests a possible
change in lead intake at that time.
Previously published analyses have not used data for all 43 subjects, particularly for
the same six subjects (labeled 15 to 20 in both experiments) who served as controls both
years. These subjects establish a baseline for non-inhalation exposures to lead, e.g., in
diet and water, and allow an independent assessment of within-subject variability over time.
EPA analyzed data for these subjects as well as others who received lead exposures of shorter
duration.
The estimated blood lead inhalation slope, 0, was calculated for each individual subject
according to the formula:
(Change in intake, jjg/day) x (mean residence time in blood, day)
P = ^
(Change in air exposure, pg/m ) x (Volume of distribution, dl)
The mean values of these parameters are given in Tables 11-13 through 11-15. The changes in
air exposure were 10.9 - 0.15 « 10.75 pg/m3 for 1970-71 and 3.2 - 0.15 = 3.05 pg/m3 in 1971-
72. Paired sample t-tests of equal means were carried out for the six controls and five sub-
jects with exposure both years, and independent sample t-tests were carried out comparing the
remaining 12 subjects the first year and nine different subjects the next year. All standard
error estimates include within-subject parameter estimation uncertainties as well as between
subject differences. The following are observations.
(1) Non-inhalation lead intake of the control subjects varied substantially during the
3
second experiment at 3.2 pg/m , with clear indication of low intake during the 14-day pre-
exposure period (net decrease of blood lead), see Figure 11-10. There was an increase in lead
intake (either equilibrium or net increase of blood lead) during the exposure period.
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KEY
~ Subject 16
Subject 16
A Subjact 17
Subject 18
O Subject 19
• Subject 20
"A A
v I / %
Y \ .
!
A fc 1 -A-
— — *4*16
40 60 80
EXPOSURE
160 180 200
POST-EXPOSURE-
EXPOSURE
TIME, days
Figure 11-10. Control subjects in Griffin experiment at 3.2 fjQlm*.
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TABLE 11-13. GRIFFIN EXPERIMENTS - SUBJECTS EXPOSED TO AIR LEAO BOTH YEARS
Subject
At 3.2
At 10.9
Mean
At 3.2
Residence
Tioe.d.
At 10.9
Change in Intake,
Post-Pre-exposure, |jg/<1*
At 3.2 At 10.9
Inhalation sloge,
pg/d£ per pg/n *
At 3.2 At 10.9
1
3
42.1 ±
17.4
55.2
±
27.2
-4.4
~
13.8
-3.0 t
12.2
0.92
±
1.94
1.09 ±0.80
2
13
47.6 ±
21.4
38.4
t
14.5
3.1
+
14.1
3.8 ±
14.6
3.95
1
3.44
1.27 ± 0.79
3
14
48.0 ±
21.7
40.1
t
15.8*
3.3
~
13.1
11.6 ±
13.4
2.50
±
2.20
1.88 ± 1.03
4
7
42.5 ±
17.6
50.1
t
22.5
12.0
~
14.2
5.1 ±
13.6
3.36
±
2.49
1.57 ± 0.99
5
4
43.6 ±
18.2
35.9
t
12.8
0.6
t
19.3
-9.5 ±
14.3
3.76
±
2.93
1.29 ± 0.68
Mean 44.7 ± 8.7
Mean w/o
subject 1 at 3.2
^Assumed volume of blood pool is 75 dl.
43.9 ± 9.4
2.9 ~ 7.2
1.6 ± 7.1
2.90 ± 1.31
3.39 t 1.44
1.42 ± 0.41
TABLE 11-14. GRIFFIN EXPERIMENTS - SUBJECTS EXPOSED TO AIR LEAO BOTH YEARS
Subject
At 3.2
Mean Residence Ti«e,d.
At 3.2 At 10.9
Change in Intake,
Post-Pre-exposure, pg/d*
At 3.2 At 10.9
Inhalation slope, .
pg/d< per pg/« *
At 3.2 At 10.9
15
16
17
18
19
20
28.6 ± 10.4
36.2 ± 14.6
33.5 l 14.0
34.4 t 15.7
36.8 t 19.6
34.0 ± 17.8
38.3 ± 21.8
35.2 t 16.8
44.2 ± 20.7
36.3 ± 18.2
49.1 ± 27.3
47.5 ± 24.0
18.6 t 11.3
5.0 ± 11.6
7.9 i 12.1
4.8 ± 11.8
-8.6 ± 13.5
2.1 ± 12.1
-3.1 ± 15.6
-7.2 ± 14.5
1.76 ± 1.17
1.57 ± 1.31
1.25 ± 1.43
0.67 ± 1.11
0.73 ± 2.82
2.90 i 2.46
-0.16 4 0.46
0.14 ± 0.35
-0.75 ±0.68
0.09 ± 0.38
-0.25 ± 0.73
-0.29 ± 0.70
Mean ± s.e.B. 34.6 ± 6.5 41.8 ~ 9.2
^Assumed volume of blood pool is 75 d£.
•10.5 ± 7.9
-2.4 ± 6.6
1.48 ± 0.84
-0.20 ± 0.27
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TABLE 11-15. GRIFFIN EXPERIMENT - SUBJECTS EXPOSED TO AIR LEAD ONE YEAR ONLY
At 3.2 (second year only) At 10.9 (first year only)
Subject
Tine, d.
Intake Change pg/d.
Slope
Subject
Tine, d.
Intake Difference, jjg/d
Slope
6
49.4 i 26.1
3.9 ± 20.1
0.52 t 3.29
1
35.3 t 15.4
5.2 ± 20.0
2.17 i 1.22
7
34.6 t 11.9
7.0 t 15.6
4.35 i 2,48
2
32.6 1 13.9
8.2 i 19.7
1.57 ± 0.95
8
38.0 t 15.2
9.4 ± 15.6
3.33 t 2.33
5
25.7 i 9.3
3.0 t 18.6
1.08 ± 0.62
9
29.7 1 9.7
3.3 ± 14.8
3.26 t 1.59
6
45.5 i 17.5
-6.4 t 12.4
1.42 t 0.76
10
40.4 ± 16.9
5.7 ± 13.9
2.08 t 1.95
8
52.0 i 22.3
1.5 t 12.9
1.90 ± 1.05
11
37.5 ± 15.3
-
3.93 ± 2.50
9
38.1 ± 14.1
7.2 t 13.7
1.67 ± 0.84
12
43.3 t 17.3
7.4 t 14;6
4.62 t 2.81
10
36.9 t 15.8
-3.9 ± 22.5
0.65 ± 1.06
14
37.9 t 14.7
-1.4 ± 16.6
3.32 t 2.25
11
30.1 t 14.3
10.3 1 15.9
1.36 ± 1.05
21
36.8 t 15.6
-7.7 ± 22.5
2.06 i 3.19
12
38.5 i 15.7
0.5 t 23.6
2.09 4 1.39
Mean
38.6 ± 5.8
3.5 ± 6.3
3.05 1 0.95
21
62.9 ± 37.2
18.6 t 16.9
1.80 1 1.40
Mean w/o
subject 6
3:37 t 0.92
23
24
43.2 ± 15.8
30.3 i 8.3
5.2 * 14,1
12.6 1 13.0
2.04 ± 0.97
1.80 t 0.65
Mean
39.3 ±6.0
5.2 f 5.4
1.63 1 0.32
-------
PRELIMINARY DRAFT
Subjects 16 and 20 had substantial increases, subjects 15 and 19 had moderate increases and
subject 18 had no increase in blood lead during exposure. Subject 17 had a marked decline in
blood lead, but the rate of decrease was much faster in the pre-exposure period, suggesting an
apparent increase of Intake during exposure periods even for this subject. These subjects had
not apparently achieved equilibrium in either blood or tissue compartments. Even though these
subjects were not exposed to air lead, the estimated difference between blood lead intake be-
fore and during exposure of the other subjects was used to calculate the apparent inhalation
slope at that exposure. The pooled inhalation slope estimated for all six controls (1.48 ±
0,82 s.e.) was significantly positive (Z = 1.76, one-tailed p <0.05), as shown in Table 11-16.
No explanation for the increased lead intake during the winter of 1971-72 can be advanced at
this time, but factors such as changes in diet or changes in resorption of bone lead are
likely to have had equal effect on the lead-exposed subjects.
No statistically significant changes in the controls were found during the first experi-
3
ment at 10.9 yg/m .
(2) Among the controls, the estimated mean residence time in pool 1 was slightly longer
for the first year than the second year, 41.8 t 9.2 days vs. 34.6 ± 6.5 days, but a paired
sample Z-test found that the mean difference for the controls (7.2 ± 11.2 days) was not signi-
ficantly different from zero (see Table 11-17).
3 3
(3) Among the five subjects exposed to 10.9 yg/m the first year and 3.2 yg/m the
second year, the mean residence time in blood was almost identical (43.9 ± 9.4 vs. 44.7 ±8.7
days).
' ¦ • 3
(4) The average inhalation slope for all 17 subjects exposed to 10.9 pg/m is 1.77 t
0.37 when the slope for the controls is subtracted. The corrected Inhalation slope for all 14
3
subjects exposed to 3.2 pg/m is 1.52 ± 1.12, or 1.90 ± 1.14 without subjects 1 and 6 who were
"non-responders." These are not significantly different. The pooled slope estimate for all
subjects is 1.75 ± 0.35. The pooled mean residence time for all subjects is 39.9 i 2.5 days.
Thus, in spite of the large estimation variability at the lower exposure level, the aver-
age inhalation slope estimate and blood lead half-life are not significantly different at the
two exposure levels. This suggests that blood lead response to small changes in air lead in-
halation is approximately linear at typical ambient levels.
11.4.1.2 The Rabinowitz et al. Study. The use of stable lead Isotopes avoids many of the
difficulties encountered in the analysis of whole blood lead levels in experimental studies.
Five adult male volunteers were housed in the metabolic research wards of the Sepulveda and
Wadsworth VA hospitals in Los Angeles for extended periods (Rabinowitz et al., 1974; 1976;
1977). For much of the time they were given low-lead diets with controlled lead content, sup-
plemented by tracer lead salts at different times.
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PRELIMINARY DRAFT
TABLE 11-16. INHALATION SLOPE ESTIMATES
Group
Controls
All exposed
At 3.2 uQ/m
1.48 i 0.82
3.00 t 0.76
At 10.9 ua/m3
-0.20 ± 0.27
1.57 t 0.26
Difference
(Exposed-
controls)
1.52 t 1.12
1.77 ± 0.37
Without sub-
jects 1, 6
3.38 ± 0.79
Difference
(Exposed w/o
1,6 - control)
1.90 t 1.14
Pooled: (all subjects)
(without subjects 1,6)
1.75 l 0.35
1.78 ± 0.35
TABLE 11-
•17. MEAN RESIDENCE TIME IN BLOOD
3
3.2 pg/m
Experiment
10.9 pg/m3
Experiment
Control
34.6 * 6.5 days
41.8 ±9.2 days
Exposed
40.8 *4.4 days
40.6 t 3.6 days
Four subjects were Initially observed 1n the ward for several weeks. Each subject was in
the semi-controlled ward about 14 hours per day and was allowed outside for 10 hours per day,
allowing the blood lead concentration to stabilize.
Subjects B, D and E then spent 22 to 24 hours per day for 40, 25 and 50 days, respec-
tively, in a low lead room with total particulate and vapor lead concentrations that were much
lower than in the rt*€sW>11c wards or outside (see Table 11-18). The subjects were thereafter
exposed to Los Angeles air with much higher air lead concentrations than in the ward.
The calculated changes in lead intake upon entering and leaving the low-lead chamber are
shown in Table 11-19. These were based on the assumption that the change in total blood lead
was proportional to the change in tracer lead. The change in calculated air lead intakes
{other than cigarettes) due to removal to the clean room were also calculated independently by
the lead balance and labeled tracer siethods (Rabinowiti et al., 1976) and are consistent with
these direct estimates.
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PRELIMINARY DRAFT
TABLE 11-18. AIR LEAD CONCENTRATIONS (pg/m3) FOR TWO SUBJECTS
IN THE RABINQWITZ STUDIES
Subject A
outside (Sepulveda VA)
Average
1.8
Range
(1,2-2.4)
inside (Sepulveda VA,
airconditioned without
filter)
1.5
(1.0-2.7)
inside (Wadsworth VA,
open air room)
2.1
(1.8-2.6)
Subject B
(Wadsworth VA)
outside
2.0
(1,6-2.4)
in room (air conditioner
with filter, no purifier)
0.91
(0.4-2.1)
in room (with purifiers,
"clean air")
0.072
(0.062-0.087)
open-air room
1.9
(1.8-1.9)
organic vapor lead
outside
0.10
-
"clean air"
0.05
-
* 5-20 days exposure for each particulate lead filter
Rabinowitz and coworkers assuaied that the amount of lead in compartments within the body
evolved as a coupled system of first-order linear differential equations with constant frac-
tional transfer rates. This compartmental model was fitted to the data. This method of
analysis is described in Appendix 11A.
Blood lead levels calculated from the three compartment model adequately predicted the
observed blood lead levels over periods of several hundred days. There was no evidence to
suggest homeostasis or other mechanisms of lead metabolism not included in the model. There
was some indication (Rabinowitz et al., 1976) that gut absorption may vary from time to time.
The calculated volumes of the pool with blood lead (Table 11-19) are much larger than the
body mass of blood (about 7 percent of body weight, estimated respectively as 4.9, 6.3, 6.3,
4,6 and 6.3 kg for subjects A-E). The blood lead compartment must include a substantial mass
of other tissue.
PB11A/B
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PRELIMINARY DRAFT
TABLE 11-19. ESTIMATES OF INHALATION
SLOPE FOR RABINOWITZ STUDIES
Changes in Changes in Inhalationt Maximum++
Intake*, Volume**, Residence-!" Air Leadft Slope vg/di. Slope
Subject
pg/day
kg
Time,
, days
pg/m3
per pg/rn3
A
17 i 5*
7.4 ± 0.6
34
± 5
2.5tt
2.98 t 1.06
4.38 t 1.55
B
16 ± 3
10.0 i 0.8
40
± 5
2.0
3.56 t 0.93
5.88 i 1.54
C
15 ± 5*
10.1 ~ 1**
37
t 5
2.2tt
2.67 ± 1.04
4.16 t 1.62
D
9 ± 2
9.9 ± 1.2
40
t 5
2.0
2.02 ± 0.60
3.34 ~ 0.99
E
12 ± 2
11.3 ± 1.4
27
± 5
2.0
1.59 t 0.47
2.63 t 0.78
"From (Rabinowitz et al., 1977) Table VI. Reduced Intake by low-lead method for subjects
B, D, E, tracer method for A, balance method for C. Standard error for C is assumed by EPA
to be same as A.
**From (Rabinowitz et al., 1976) Table II. EPA has assumed standard error with coefficient
of variation same as that for quantity of tracer absorbed in Table VI, except for subject C.
tEstimates from (Rabinowitz et al., 1976) Table II. Standard error estimate from combined
sample.
ttSee text, For A and C, estimated from average exposure. For B, D, £ reduced by 0.2 pg/ii)3
for clean room exposure. Coefficient of variation assumed to be 10%.
~Assumed density of blood 1.058 g/cm3.
~~Assuming outside air exposure is 2.1 pg/m3 rather than 4 pg/m3 for 10 hours.
The mean residence time in blood in Table 11-19 includes both loss of lead from blood to
urine and transfer of a fraction of blood lead to other tissue pools. This parameter reflects
the speed with which blood lead concentrations approach a new quasi-equilibrium level. Many
years may be needed before approaching a genuine equilibrium level that includes lead that can
be mobilized from bones.
One of the greatest difficulties in using these experiments is that the air lead ex-
posures of the subjects were not measured directly, either by personal monitors or by restric-
ting the subjects to the metabolic wards. The times when the subjects were allowed outside
the wards included possible exposures to ground floor and street level air, whereas the outside
air lead monitor was mounted outside the third-floor window of the ward. The VA hospitals are
not far from major streets and the subjects' street level exposures could have been much
higher than those measured at about 10 m elevation (see Section 7.2.1.3). Some estimated
ratios between air concentrations at elevated and street level sites are given in Table 7.6.
3
A second complication is that the inside ward value of 0.97 yg/m (Rabinowitz et al.,
1977) used for subject B may be appropriate for the Wadsworth VA hospital, but not for subject
PB11A/B
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PRELIMINARY DRAFT
A in the Sepulveda VA hospital (see Table 11-18). The change In air lead values shown in
Table 11-19 is thus nominal, and is likely to have systematic inaccuracies much larger than
the nominal 10 percent coefficients of variation stated. The assumption is that for subjects
B, D and E, the exposure to street level air for 10 hours per day was twice as large as the
3
measured roof level air, i.e., 4 pg/m ; the remaining 14 hours per day was at the ward
3 3
level of 0.97 pg/m ; thus the time-averaged level was (10 x 4 + 14 x 0.97)/24 = 2.23 jjg/m .
The average controlled exposure during the "clean room" part of the experiment was 23, 22 and
24 hours respectively for subjects B, 0, E; thus averaged exposures were 0.19, 0.28, and 0.12
pg/m , and reductions in exposure were about 2.0 pg/n . This value is used to calculate the
slope. For subject A, the total intake due to respired air is the assumed indoor average of
J
1.5 pg/m for the Sepulveda VA hospital, combining indoor and outdoor levels (10 x 4 + 14 x
I.5)/24 = 2.54 For subject C we use the Wadsworth average. Apart from uncertainties in
the air lead concentration, the inhalation slope estimates for Rabinowitz's subjects have less
internal uncertainty than those calculated for subjects in Griffin's experiment.
The inhalation slopes thus calculated are the lowest that can be reasonably derived from
this experiment, since the largest plausible air lead concentrations have been assumed. The
third-floor air monitor average of 2.1 pfl/n3 is a plausible minimum exposure, leading to the
higher plausible maximum inhalation slopes in the last column of Table 11-19. These are based
on the assumption that the time-averaged air lead exposure 1s smaller by 10x(4-2.1)/24 = 0.79
pg/m3 than assumed previously. It is also possible that some of this difference can be
attributed to dust ingestion while outside the metabolic ward.
II.4.1.3 The Chamberlain et al. Study. A series of investigations were carried out by
A.C. Chamberlain et al. (1975a,b; 1978) at the U.K. Atomic Energy Research Establishment in
Harwell, England. The studies included exposure of up to 10 volunteer subjects to inhaled,
ingested and injected lead in various physical forms. The inhalation exposures included labo-
ratory inhalation of lead aerosols generated in a wind tunnel, or box, of various particle
sizes and chemical compositions (lead oxide and lead nitrate). Venous blood samples were
taken at several times after inhalation of 203Pb. Three subjects also breathed natural high-
way exhaust fumes at various locations for times up to about 4.5 hours.
The natural respiratory cycles in the experiments varied from 5.7 to 17.6 seconds (4 to
11 breaths per minute) and tidal volumes from 1.6 to 2.3 liters. Lung deposition of lead-
bearing particles depended strongly on particle size anc composition, with natural exhaust
particles being more efficiently retained by the lung (30 to 50 percent) than were the chem-
ical compounds (20 to 40 percent).
The clearance of lead from the lungs was an extended process over time and depended on
particle size and composition, leaving only about 1 percent of the fine wind tunnel aerosols
PB11A/B
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PRELIMINARY DRAFT
in the lung after 100 hours, but about 10 percent of the carbonaceous exhaust aerosols. The
203Pb isotope reached a peak blood level about 30 hours after inhalation, the blood level then
representing about 60 percent of the initial lung burden.
A substantial fraction of the lead deposited in the lung appears to be unavailable to the
blood pool in the short terra, possibly due to rapid transport to and retention in other tis-
sues including skeletal tissues. In long term balance studies, some of this lead in deep tis-
sue compartment would return to the blood compartment.
lead kinetics were also studied by use of injected and ingested tracers, which suggested
that in the short term, the mean residence time of lead in blood could be calculated from a
one-pool model analysis.
Chamberlain et al. (1978) extrapolated these high level, short term exposures to longer
term ones. The following formula and data were used to calculate a blood-to-air level ratio:
[Ti/2] [X Deposition] [% Absorption] [Daily ventilation]
p = [Blood volume] [0.693]
where. j ^ _ bi0T0gjcai half life
With an estimated value of T^ = 18 days (mean residence time T^/0.693 = 26 days), with SO
percent for deposition in lung for ordinary urban dwellers, and 55 percent of the lung lead
retained in the blood lead compartment (all based on Chamberlain's experiments), with an
3
assumed ventilation of 20 m /day over blood volume 5400 ml (Table 10.20 in Chamberlain et
al., 1978), then
p - 26 day X 0.50 X 0.55 X 20 m3/day _ 2 ? B3/dl
54 dl
This value of p could vary for the following reasons,
1. The absroption from lung to blood used here, 0.55, refers to short term kine-
tics. In the long term, little lead is lost through biliary or pancreatic
secretions, nails, hair and sweat, so that most of the body lead is available to
the blood pool even if stored in the skeleton from which it may be resorbed.
Chamberlain suggests an empirical correction to 0.55 X 1.3 = 0.715 absorption.
2. The mean residence time, 26 days, is shorter than in Rabinowitz's subjects, and
the blood volume is less, 54 dl. It is possible that in the Rabinowitz study,
PB11A/B 11-49 7/29/83
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PRELIMINARY Df#T
the mean times are longer and the blood pool size (100 dl) 1s larger than here
because Rabinowitz et al. Included relatively less labile tissues such as kidney
and liver in the pool. Assuming 40 days mean residence time and 100 dl blood
volume the slope can be recalculated,
„ _ 40 d X 0.50 X 0.55 X 20 m3/d _ „ „ _3^,
p iQo di 2.2 m /dl
3. The breathing rate could be much less, for inactive people.
11.4.1.4 The Kehoe Study. Between 1950 and 1971, Professor R. A. Kehoe exposed 12 subjects
to various levels of air lead under a wide variety of conditions. Four earlier subjects had
received oral Pb during 1937-45. The inhalation experiments were carried out in an inhalation
chamber at the University of Cincinnati, in which the subjects spent varying daily time
periods over extended intervals. The duration was typically 112 days for each exposure level
in the inhalation studies, at the end of this period it was assumed the blood lead concentra-
tion had reached a near equilibrium level. The experiments are described by Kehoe (1961a,b,c)
and the data and their 'analyses by Gross (1981) and Hammond et al. (1981). The studies most
relevant to this document are those in which only particles of lead sespuioxide aerosols in
the submicron range were used, so that there was at least one air lead exposure (other than
control) for which the time-averaged air lead concentration did not exceed 10 Only six
subjects met these criteria: LD (1960-63), JOS (1960-63), NK (1963-66), SS (1963-68), HR
(1966-67) and DH (1967-69). Subject OH had a rather high initial lead concentration (30
(jg/dl) that fell during the course of the experiment to 28 yg/dl; apparently daily detention
in the inhalation chamber altered OH's normal pattern of lead exposure to one of lesser total
exposure. The Kehoe studies did not measure non-experimental airborne lead exposures, and
did not measure lead exposures during "off" periods. Subject HR received three exposure
levels from 2.4 to 7.5 pg/m3, subject NK seven exposure levels from 0.6 to 4.2 jjg/m3 and sub-
jects SS 13 exposure levels from 0.6 to 7.2 jjg/m3, LD and JOS were each exposed to about 9,
19, 27 and 36 pg/®3 during sequential periods of 109-113 days.
A great deal of data on lead content in blood, feces, urine and diet were obtained in
these studies and are exhibited graphically in Gross (1979) (see Figure 11-11). Apart from
the quasi-equilibrium blood lead values and balances reported in Gross (1979; 1981), there has
been little use of these data to study the uptake and distribution kinetics of lead in man.
EPA analyses used only the summary data in Gross (198!ry.
Data from Gross (1981) were fitted by least squares linear and quadratic regression
models. The quadratic models were not significantly better than the linear model except for
PB11A/B
11-50
7/29/83
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m
h-»
£
X
CO
\o
CO
C*i
SUBJECT - SS
ImIMlJUb
>.
200
?i iS
i
2
BE
ft.
<
HI
j
-»
i| i5
+ 0 j->
a 2
760. ink), jsoo. 1000.11100.1300. iabo. 1400] wboji«Ao. j 70O.C
if i«y 1
.•j
& <
011*
~ i
CO Ml
>>
<<
OO
&
o
99
sis S £» Sf iu 8 _ ____ _
TIME (days*
Figure 11-11. Data plots for individual subjects with time for kehoe data as presented by Gross.
ao
m
as
>
30
-<
o
30
>
-------
PRELIMINARY DRAFT
subjects LD and JOS, who were exposed to air levels above 10 |jg/ms. The linear terms predomi-
nate in all models for air lead concentrations below 10 pg/m3 and are reported in Table 11-20.
These data represent most of the available experimental evidence in the higher range of
ambient exposure levels, approximately 3 to 10 pg/m3.
Data for the four subjects with statistically significant relationships are shown in
Figure 11-12, along with the fitted regression curve and its 95 percent confidence band.
TABLE 11-20. LINEAR SLOPE FOR BLOOD LEAD VS. AIR LEAD AT
LOW AIR LEAD EXPOSURES IN KEHOE'S SUBJECTS
SUBJECT
LINEAR SLOPES p,
LINEAR MODEL
m3/dl» i s.e.
QUADRATIC MODEL
RANGE
AIR*
BLOOD
DH®
HR .
J0Sb
lob
NK
SSC
-0.34 ± 0.28
0.70 i 0.46
0.67 t 0.07
0.64 ± 0.11
2.60 ± 0.32
1.31 4 0.20
0.14 ± 1.25
0.20 ± 2.14
1.01 ± 0.19
1.29 t 0.06
1.55 ± 1.28
1.16 ± 0.78
5.6
2.4
9.4
9.3
0.6
0.6
- 8.8
- 7.5
- 35.7
- 35.9
- 4.0
- 7.2
26 - 31
21 - 27
21 - 46
18 - 41
20 - 30
18 - 29
*Also control = 0
aNo statistically significant relationship between air and blood lead.
bHigh exposures. Use linear slope from quadratic model.
cLow exposures. Use linear slope from linear model.
11.4.1.5 The Azar et al. Study. Thirty adult male subjects were obtained from each of five
groups: 1) Philadelphia cab drivers; 2) DuPont employees in Starke, Florida; 3) DuPont
employees 1n Barksdale, Wisconsin; 4) Los Angeles cab drivers; and 5) Los Angeles office
workers (Azar et al., 1975). Subjects carried air lead monitors in their automobiles and in
their breathing zones at home and work. Personal variables (age, smoking habits, water
samples) were obtained from all subjects, except for water samples from Philadelphia cab
drivers. Blood lead, ALAD urine lead and other variables were measured. From two to eight
blood samples were obtained from each subject during the air monitoring phase. Blood lead
determinations were done in duplicate. Table 11-21 presents the geometric means for air lead
and blood lead.for the five groups. The geometric means were calculated by EPA from the raw
data presented 1n the authors' report (Azar et al., 1975).
The Azar study has played an important role in setting standards because of the care used
in measuring air lead in the subjects' breathing zone. Blood lead levels change in response
to air lead levels, with typical time constants of 20 to 60 days. One must assume that the
subjects' lead exposures during preceding months had been reasonably similar to those during
PB11A/B 11-52 7/29/83
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PRELIMINARY DRAFT
1
Q
O
o
SUBJECT NK
1 2 3
AIR LEAD, nglm*
at 30
i
!
o
s
£
I FTr
SUBJECT SS
AIR LEAD, fig/m*
SUBJECT LD
0 G 10 16 20 25 30 36
AIR LEAD, fjg/m'
0 5 10 15 20 2B 30
AIR LEAD, pg/m'
PB11A/B
Figure 11-12. Blood level vs. air lead relationships for kehoe inhalation studies; linew rela-
tion for low exposures, quadratic for high exposures, with 9S% confidence bands
11-53 7/29/83
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PRELIMINARY DRAFT
TABLE 11-21. GEOMETRIC MEAN AIR AND BLOOD LEAD LEVELS (pg/100 g)
FOR FIVE CITY-OCCUPATION GROUPS (DATA CALCULATED BY EPA)
Geometric mean Geometric mean
air lead, blood lead, Sample
Group Mfl/n>3 GSO Mfl/100 g GSD size Code
Cab drivers
Philadelphia, PA
2.59
1.16
22.1
1.16
30
C1
Plant employees
Starke, FL
0.59
2.04
15.4
1.41
29
C2
Plant employees
Barksdale, WI
0.61
2.39
12.8
1.43
30
C3
Cabdrivers
Los Angeles, CA
6.02
1.18
24.2
1.20
30
C4
Office workers
Los Angeles, CA
2.97
1.29
18.4
1.24
30
C5
Source: Azar et al. (1975).
the study period. Models have been proposed for these data by Azar et al. (1975), Snee (1981;
198%) and Hammond et al. (1981) Including certain nonlinear models.
Azar et al. (1975) used a log-log model for their analysis of the data. The model in-
cluded dummy variables, C^, C2, Cg, C^, Cg, which take on the value 1 for subjects in that
group and 0 otherwise (see Table 11-21 for the definitions of these dummy variables). The
fitted model using natural logarithms was
log (blood Pb) » 2.951 Cj + 2.818 C? +
2.627 C3 + 2.910 C# + 2.821 Cg * 0.153 log (air Pb)
This model gave a residual sun of squares of 9.013, a mean square error of 0,63 (143 degrees
of freedom), and a multiple R2 of 0.502. The air lead coefficient had a standard error of
0.040. The fitted model Is nonlinear in air lead, and so the slope depends on both air lead
and the Intercept. Using an average intercept value of 1.226, the curve has a slope ranging
3 3
from 10.1 at an air lead level of 0.2 yg/m to 0.40 at an air lead level of 9 jjg/m .
PB11A/8
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Snee (1982b) reanalyzed the same data and fitted the following power function model,
log (blood Pb) = log [12.1 (air Pb + 6.00 + 1.46 C2
~ 0.44 C3 + 2.23 C4 + 6.26 C5)0"2669]
This model gave a residual sum of squares of 9.101, a mean square error of 0.064 (142 degrees
of freedom) and a multiple R2 of 0.497. Using an average constant value of 3.28, the slope
ranges from 1.29 at an air lead of 0.2 to 0.51 at an air lead of 9.
An important extension in the development of models for the data was the inclusion of
separate non-air contributions or background exposures for each separate group. The coeffi-
cients of the group variables, C^, in the lead exposure model may be interpreted as measures
of total exposure of that group to non-air external sources (cigarettes, food, dust, water)
and to endogenous sources (lead stored in skeleton). Water and smoking variables were used to
estimate some external sources. (This required deleting another observation for a subject
with unusually high water lead.) The effect of endogenous lead was estimated using subject
age as a surrogate measure of cumulative exposure, since lead stored in skeleton is known to
increase approximately linearly with age, for ages 20 to 60 (Gross et al., 1975; Barry, 1975;
Steenhout, 1982) in homogeneous populations.
In order to facilitate comparison with the constant 0 ratios calculated from the clinical
studies, EPA fitted a linear exposure model to the Azar data. The model was fitted on a loga-
rithmic scale to facilitate comparison of goodness of fit with other exposure models and to
produce an approximately normal pattern of regression residuals. Neither smoking nor water
lead provided significantly better fits to the log (blood lead) measurements after the effect
of age was removed.
Age and air lead may be confounded to some extent because the regression coefficient for
age may include the effects of prior air lead exposures on skeletal lead buildup. This would
have the effect of reducing the estimated apparent slope p.
Geometric mean regressions of blood lead on air lead were calculated by EPA for several
assumptions: (i) A linear model analogous to Snee's exposure model, assuming different non-
air contributions in blood lead for each of the five subgroups; (ii) linear model in which age
of the subject is also used as a surrogate measure of the cumulative body burden of lead that
provides an endogenous source of blood lead; (iii) linear model similar to (ii), in which the
change of blood lead with age is different in different subgroups, but it is assumed that the
non-air contribution is the same in all five groups (as was assumed in the 1977 criteria docu-
ment); (iv) linear model in which both the non-air background and the change in blood lead
PB11A/B
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PRELIMINARY DRAFT
with age may differ by group; and (v) nonlinear model similar to (iv). None of the fitted
models are significantly different from each other using statistical tests of hypotheses about
parameter subsets in nonlinear regression (Gallant, 1975).
11.4.1.6 Silver Vallev/Kellogg. Idaho Study. In 1970, EPA carried out a study of a lead
smelter in Kellogg, Idaho (Hammer et al., 1972; U.S. Environmental Protection Agency, 1972).
The study was part of a national effort to determine the effects of sulfur dioxide, total sus-
pended particulate and suspended sulfates, singly and in combination with other pollutants, on
human health. It focused on mixtures of the sulfur compounds and metals. Although it was
demonstrated that children had evidence of lead absorption, insufficient environmental data
were reported to allow further quantitative analyses.
In 1974, following the hospitalization of two children from Kellogg with suspected acute
lead poisoning, the CDC joined the State of Idaho in a comprehensive study of children in the
Silver Valley area of Shoshone County, Idaho, near the Kellogg smelter (Yankel et al., 1977;
Landrigan et al., 1976).
The principal source of exposure was a smelter whose records showed that emissions aver-
aged 8.3 metric tons per month from 1955 to 1964 and 11.7 metric tons from 1965 to September
1973. After a September 1973 fire extensively damaged the smelter's main emission filtration
facility, emissions averaged 35.3 metric tons from October 1973 to September 1974 (Landrigan
et al., 1976). The smelter operated during the fall and winter of 1973-74 with severely limited
air pollution control capacity. Beginning in 1971, ambient concentrations of leacl in the
vicinity of the smelter were determined from particulate matter collected by Hi-Vol air
samples. Data indicated that monthly average levels measured in 1974 (Figure 11-13) were
three to four times the levels measured in 1971 (von Lindern and Yankel, 1976). Individual
exposures of study participants to lead in the air were estimated by interpolation from these
data. Air lead exposures ranged from 1.5 pg/m3 to 30 (jg/m3 monthly average (see Figure 11-13).
Soil concentrations were as high as 24,000 pg/g and averaged 7000 pg/g within one mile of the
smelter. House dusts were found to contain as much as 140,000 pg/g and averaged 11,000 pg/g
in homes within one mile of the complex.
The study was initiated in May of 1974 and the blood samples were collected in August
1974 from children 1 to 9 years old in a door-to-door survey (greater than 90 percent partici-
pation). Social, family and medical histories were conducted by interview. Paint, house
dust, yard and garden soils, grass, and garden vegetable samples were collected. At that
time, 385 of the 919 children examined (41.9 percent) had blood lead levels in excess of 40
pg/dl, 41 children (4.5 percent) had levels greater than 80 pg/dl. All but 2 of the 172
children living within 1.6 km of the smelter had levels greater than or equal to 40 pg/dl.
Those two children had moved into the area less than six months earlier and had blood lead
PB11A/B
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LNIIIIIIIIIIIIiaHMjL
TIME, y««r
Figure 11-13. Monthly ambient air lead concentrations in Kellogg, Idaho,
1971 through 1878.
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PRELIMINARY DRAFT
levels greater than 35 pg/dl. Both the mean blood lead concentration and the number of chil-
dren classified as exhibiting excess absorption, decreased with distance from the smelter
(Table 11-22). Blood lead levels were consistently higher in 2- to 3-year-old children than
they were in other age groups (Table 11-23). A significant negative relationship between
blood lead level and hematocrit value was found. Seven of the 41 children (17 percent) with
blood lead levels greater than 80 pg/dl were diagnosed as being anemic on the basis of
hematocrit less than 33 percent, whereas only 16 of 1006 children (1.6 percent) with blood
lead levels less than 80 pg/dl were so diagnosed. Although no overt disease was observed in
children with higher 4ead intake, differences were found in nerve conduction velocity.
Details of this finding are discussed in chapter 12.
Yankel et al. (1977) fitted the data to the following model:
In (blood lead) = 3.1 ~ 0.041 air lead + 2.1 x 10 ^ soil lead
+ 0.087 dustiness - 0.018 age
~ 0.024 occupation
where air lead was in mo/*3; soil lead was in pg/g; dustiness was 1, 2 or 3; age was in years;
and occupation was a Hollingshead index. The analysis included 879 subjects, had a multiple
R of 0.622 and a residual standard deviation of 0.269 (geometric standard deviation of 1.31).
Walter et al. (1980) used a similar model to examine age specific differences of the re-
gression coefficients for the different variables. Those coefficients are summarized in Table
•11-24. The variable that was most significant overall was air lead; its coefficient was ap-
proximately the same for all ages, corresponding to a change in blood lead of about 1 pg/dl
per unit increase of air lead (in pg/m3) at an air exposure of 1 pg/m3 and about 2.4 pg/dl per
unit increase in air at an air exposure of 22 (jg/m3.
The next most important variable that attained significance at a variety of ages was the
household dustiness level (coded as low = 0, medium = 1 or high = 2), showing a declining ef-
fect with age and being significant for ages 1 to 4 years. This suggested age-related hygiene
behavior and a picture of diminishing home orientation as the child develops. For ages 1 to 4
years, the coefficient indicates the child in a home with a "medium" dust level would have a
blood lead level ~ 10 percent higher than a child in a home with a "low" dust level, other
factors being comparable.
The coefficients for soil lead-blood lead relationships exhibited a fairly regular pat-
tern, being highly significant (p <0.01) for ages 3 to 6 years, and significant (p <0.05) at
ages 2 to 6 years. The maximum coefficient (at age 6) indicates a 4 percent increase in blood
lead per 1000 pg/g increase in soil lead.
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TABLE 11-22. GEOMETRIC MEAN BLOOD LEAO LEVELS BY AREA COMPARED WITH
ESTIMATED AIR-LEAD LEVELS FOR 1- TO 9-YEAR-OLD CHILDREN
LIVING NEAR IDAHO SMELTER. (GEOMETRIC STANDARD DEVIATIONS,,
SAMPLE SIZES AND OISTANCES FROM SMELTER ARE ALSO GIVEN)
Area
Geometric mean
blood lead,
Mfl/dl
GSD
Sample
size
X blood
lead
>40fjg/d1
Estimated
air lead,
MS/"3
Distance from
smelter, km
1
65.9
1.30
170
98.9
18.0
0- 1.6
2
47.7
1.32
192
72.6
"14.0
1.6- 4.0
3
33.8
1.25
174
21.4
6.7
4.0-10.0
4
32.2
1.29
156
17.8
3.1
10.0-24.0
5
27.5
1.30
188
8.8
1.5
24.0-32.0
6
21.2
1.29
90
1.1
1.2
about 75
aEPA analysis of data from Yankel et al. (1977).
TABLE 11-23. GEOMETRIC MEAN BLOOD LEAO LEVELS BY AGE AND AREA FOR
SUBJECTS LIVING NEAR THE IDAHO SMELTER
Area
1
2
3
4
5
Age Group
6 7 8
9
Teenage
Adult
1
69*
72
75
75
68
66
63
60
57
39
37
2
50
51
55
46
49
50
47
42
40
33
33
3
33
36
36
35
35
35
31
32
32
28
30
4
31
35
34
31
31
35
30
32
30
34
5
27
35
29
29
29
28
25
27
24
32
6
21
25
22
23
20
22
20
22
17
7
28
30
28
32
30
26
37
30
20
35
32
"error in original publication (Yankel et al., 1977).
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TABLE 11-24. AGE SPECIFIC REGRESSION COEFFICIENTS FOR THE ANALYSIS OF
LOG-BLOOD-LEAD LEVELS IN THE IDAHO SMELTER STUDY
Age
Air
Dust
Occupation
Pica
Sex
Soil (xl0«)
Intercept
N
1
0.0467*
0.119t
0.0323
0.098
0.055
3.5
3.017
98
2
0.0405*
0.106t
0.0095
0.225*
0.002
20.6t
3.567
94
3
0.0472*
0.108T
0.0252
0.077
0.000
24.2*
3.220
115
4
0.0366*
0.107f
0.0348
0.117
0.032
32.1*
3.176
104
5
0.0388*
0.052
0.0363f
0.048
-0.081
23.4*
3.270
130
6
0.0361*
0.070
0.0369t
0.039
-0.092
38.4*
3.240
120
7
0.0413*
0.053
0.0240
0.106
-0.061
21.3f
3.329
113
8
0.0407*
0.051
0.04221"
0.010
-0.106f
16.2
3.076
105
9
0.0402*
o.osit
0.0087
0.108
-0.158*
11.6
3.477
104
* p <0.01
t P <0.05
Pica (coded absent = 0, present = 1) had a significant effect at age 2 years, but was in-
significant elsewhere; at age 2 years, an approximate 25 percent elevation in blood lead is
predicted in a child with pica, compared with an otherwise equivalent child without pica.
Occupation was significant at ages 5, 6 and 8 years; at the other ages, however, the sign
of the coefficient was always positive, consistent with a greater lead burden being introduced
into the hone by parents working in the smelter complex.
Finally, sex (coded male = 0; female = 1) had a significant negative coefficient for ages
8 and 9 years, indicating that boys would have lead levels 15 percent higher than girls at
this age, on the average. This phenomenon 1s enhanced by similar, but nonsignificant, nega-
tive coefficients for ages 5 to 7 years.
Snee (1982c) also reanalyzed the Idaho smelter data using a log-linear model. He used
dummy variables for age, work status of the father, educational level of the father, and
household dust level (cleanliness). The resulting model had a multiple R* of 0.67 and a resi-
dual standard deviation of 0.250 (geometric standard deviation of 1.28). The model showed
that 2-year-olds had the highest blood lead levels. The blood lead inhalation slope was es-
sentially the same as that of Yankel et al. (1977) and Walter et al. (1980).
The above non-linear analyses of the Idaho smelter study are the only analyses which sug-
gest that the blood lead to air lead slope increases with increasing air lead, a finding in
counterdlst1 nct1 on to the findings of decreasing slopes seen at high air lead exposures in
other studies. An alternative to this would be to attempt to fit a linear model as described
1n Appendix 11-B. Exposure coefficients were estimated for each of the factors shown In
Table 11-25. The results for the different covariates are similar to those of Snee (1982c)
and Walter et al. (1980).
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TABLE 11-25. ESTIMATED COEFFICIENTS* AND STANDARD
ERRORS FOR THE IDAHO SMELTER STUDY
Asymptotic
Factor Coefficient Standard Error
Intercept (yg/dl)
13.19
1.90
Air lead (pg/m^)
1.53
0.064
Soil lead (1000 pg/g)
1.10
0.14
Sex (male=1, female=0)
1.31
0.59
Pica (eaters=l, noneaters=0)
2.22
0.90
Education (graduate training=0)
At least high school
3.45
1.44
No high school
4.37
1.51
Cleanliness of home (clean*0)
Moderately clean
3.00
0.65
Dirty
6.04
1.06
i
Age (1 year olds=0)
2 years olds
4.66
1.48
3 years olds
5.48
1.32
4 years olds
3.16
1.32
5 years olds
2.82
1.25
6 years olds
2.74
1.24
7 years olds
0.81
1.23
8 years olds
-0.19
1.28
9 years olds
-1.50
1.21
Work status (no exposure=0)
-
Lead or zinc worker
3.69
0.61
Residual standard deviation = 0.2576 (geometric standard deviation = 1.29)
Multiple R2 = 0.662
Number of observations = 860
"Calculations made by EPA
Because the previous analyses noted above indicated a nonlinear relationship, a similar
model with a quadratic air lead term added was also fitted. The coefficients for the other
factors remained about the same, and the improvement in the model was marginally significant
3
(p = 0.05). This model gave a slope of 1.16 at an air lead of 1 pg/m , and 1.39 at an air
lead of 2 pg/m^. Both the linear and quadratic models, along with Snee's (1982) model are
shown in Figure 11-14. The points represent mean blood lead levels adjusted for the factors
in Table 11-25 (except air lead) for each of the different exposure subpopulations.
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PRELIMINARY DRAFT
Yankel et al. (1977), Walter et at. (1980) and Snee (1982c) make reference to a follow-up
study conducted in 1975. The second study was undertaken to determine the effectiveness of
control and remedial measures instituted after the 1974 study. Between August 1974 and August
1975, the mean annual air lead levels decreased at all stations monitored. In order of in-
creasing distance from the smelter, the annual mean air lead levels for the one year preceding
each drawing were 18.0 to 10.3 M9/®3. 14*° to Mg/m3. 6,7 to 4.9 yg/m3 and, finally 3.1 to
2.5 n9/®3 at 10 to 24 km. Similar reductions were noted in house dust lead concentrations.
In a separate report, von lindern and Yankel (1976) described reductions in blood lead levels
of children for whom determinations were made in both years. The results demonstrated that
significant decreases in blood lead concentration resulted from exposure reductions.
I I I I I I I I I I I I I I I I I I I II
m
o
20
10
0
LINEAR (EPA)
— QUADRATIC (EPAJ
LOG-LINEAR (SNEE)
~l I I I I l I I
10 16
AIR LEAD, fig/m*
20
25
Figure 11*14. Fitted aquations to Kellogg Idaho/Silver Valley
adjusted blood lead data.
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11.4.1.7 Omaha. Nebraska Studies. Exposure from both a primary and secondary smelter in the
inner city area of Omaha, Nebraska, has been reported in a series of publications (Angle et
al., 1974; Angle and Mclntire, 1977; Mclntire and Angle, 1973). During 1970 to 1977 children
were studied from: an urban school at a site immediately adjacent to a small battery plant
and downwind from two other lead emission sources; from schools in a mixed commercial-residen-
tial area; and from schools in a suburban setting. Children's blood lead levels were obtained
by macro technique for 1970 and 1971, but Delves micro assay was used for 1972 and later. The
differences for the change in techniques were taken into account in the presentation of the
data. Air lead values were obtained by Hi-Vol samplers and dustfall values were also moni-
tored. Table 11-26 presents the authors' summary of the entire data set, showing that as air
lead values decrease and then increase, dustfall and blood lead values follow. The authors
used regression models, both log-linear and semilog, to calculate (air lead)/(blood lead).
Specific reports present various aspects of the work. Black children in the two ele-
mentary schools closest to the battery plant had higher blood leads (34.1 pg/dl) than those in
elementary and junior high schools farther away (26.3 pg/dl). Best estimates of the air ex-
posures were 1.65 and 1.48 pg/m , respectively (Mclntire and Angle, 1973). The latter study
compared three populations: urban vs. suburban high school students, ages 14 and 18; urban
black children, ages 10 to 12, vs. suburban whites, age 10 to 12; and blacks ages 10 to 12
with blood lead levels over 20 pg/dl vs. schoolmates with blood lead levels below 20 pg/dl
(Angle et al., 1974). The urban vs. suburban high school children did not differ significan-
tly, 22.3 ±1.2 and 20.2 ±7.0 pg/dl, respectively, with mean values of air lead concentra-
tions of 0.43 and 0.29 pg/m . For 15 students who had environmental samples taken from their
homes, correlation coefficients between blood lead levels and soil and housedust lead levels
were 0.31 and 0.29, respectively.
Suburban 10-to-12-year-olds had lower blood lead levels than their urban counterparts,
17.1 ± 0.7 versus 21.7 ± 0.5 pg/dl (Angle et al., 1974). Air lead exposures were higher in
the urban than in the suburban population, although the average exposure remained less than 1
3 2
pg/m . Dustfall lead measurements, however, were very much higher; 32.96 mg/m /month for
2
urban 10-to-12-year-olds vs. 3.02 mg/m /month for suburban children.
Soil lead and house dust lead exposure levels were significantly higher for the urban
black high lead group than for the urban low lead group. A significant correlation (r = 0.49)
between blood lead and soil lead levels was found.
Angle has reanalyzed the Omaha study using all of the data on children. There were 1075
samples from which blood lead (pg/dl), air (pg/m3), soil (pg/g) and house dust (pg/g) lead
were available. The linear regression model, fitted in logarithmic form, was
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Pb-Blood = 15.'67 + 1.92 Pb-Air ~ 0.00680 Pb-Soil + 0.00718 Pb-Mouse Oust
(±0.40) (±0.60) (±0.00097) (±0.00090)
(N = 1075, R2 = 0.20, S2 = 0.0901, GSD = 1.35)
Similar models fitted by age category produced much more variable results, possibly due to
snail ranges of variation in air lead within certain age categories.
TABLE 11-26. AIR, 0USTFALL AND BLOOD LEAD CONCENTRATIONS IN
OMAHA, NE STUDY, 1970-1977*
Air
Dustfall,
Blood,
Group
jig/m (N) pg/m - mo (N)c
MO/dl (N)d
All urban children, nixed commercial and residential site
1970-71 1.48 ± 0.14(7;65)
1972-73 0.43 ± 0.08(8;72) 10.6 t 0.3(6)
1974-75 0.10 ± 0.03(10;72) 6.0 ± 0.1(4)
1976-77 0.52 t 0.07(12;47) 8.8 (7)
31.4 i 0.7(168)
23.3 ± 0.3(211)
20.4 t 0.1(284)
22.8 ± 0.7(38)
Children at school in
a commercial site
1970-71
1972-73
1974-75
1976-77
1.69 ± 0.11(7;67)
0.63 ± 0.15(8;74)
0.10 ± 0.03(10;70)
0.60 t 0.10(12;42)
25.9 ± 0.6(5)
14.3 t 4.1(4)
33.9 (7)
34.6 ± 1.5(21)
21.9 ± 0.6(54)
19.2 ± 0.9(17)
22.8 ± 0.7(38)
All suburban children
in a residential site
1970-71
1972-73
1974-75
1976-77
0.79 ± 0.06(7;65)
0.29 ± 0.04(8;73)
0.12 ± 0.05(10;73)
4.6 ± 1.1(6)
2.9 t 0.9(4)
19.6 ± 0.5(81)
14.4 ± 0,6(31)
18.2 ± 0.3(185)
Blood lead 1970-71 1s by the macro technique, corrected for an established
laboratory bias of 3 pg/dl> macro-micro; all other values are by Delves micro
assay.
* Number of months; number of 24-hour samples.
CN * Number of months.
* Number of blood samples.
Source: Adapted from Angle and Mclntire, 1977.
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11.4.1.8 Roels et al. Studies. Roels et al. (1976, 1378, 1980) have conducted a series of
studies in the vicinity of a lead smelter in Belgium. Roels et al. (1980) reports a follow-up
study (1975) that included study populations from a rural-nonindustrialized area as well as
from the lead smelter area. The rural group consisted of 45 children (11-14 years). The
smelter area group consisted of 69 school children from three schools. These children were
divided into two groups; group A (aged 10-13) lived less than 1 km from the smelter and their
schools were very close to the smelter; group B consisted of school children living more than
1.5 km from the smelter and attending a school more distant from the smelter.
In 1974 the smelter emitted 270 kg of lead and the air lead levels were 1 to 2 orders of
magnitude greater than the current Belgian background concentration for air lead (0.23 pg/m^).
Soil and vegetation were also contaminated with lead; within 1 km the soil lead level was
12,250 yg/g. The concentration of lead in drinking water was less than 5 iig/1.
Environmental assessment included air, soil and dust. Air monitoring for lead had been
continuous since September 1973 at two sites, one for each of the two groups. In the rural
area, air monitoring was done at two sites for five days using membrane pumps. Lead was ana-
lyzed by flameless atomic absorption spectrophotometry. Dust and soil samples were collected
at the various school playgrounds. The soil sample was analyzed by flameless atomic absorp-
tion,
A 25 ml blood sample was collected from each child and immediately divided among three
tubes. One tube was analyzed for lead content by flameless atomic absorption with background
correction. Another tube was analyzed for ALA-D activity while the third was analyzed for FEP.
FEP was determined by the Roels modification of the method of Sassa. ALA-0 was assayed by the
European standard method.
Air lead levels decreased from area A to area B. At both sites the airborne lead levels
declined over the two years of monitoring. The amount of lead produced at this smelter during
this time remained constant, about 100,000 tons/year. The median air lead level at the closer
3
site (A) dropped from 3.2 to 1.2 pg/m , while at the far site (B) the median went from 1.6 to
0.5-0.8 pg/m . The rural area exposure levels did not vary over the study period, remaining
rather constant at about 0.30 Hg/m3.
Both smelter vicinity groups showed signs of increased lead absorption relative to the
rural population. Blood lead levels for group A were about three times those for the rural
population (26 pg/dl vs. 9 pg/dl). The former blood lead levels were associated with about a
50 percent decrease in ALA-D activity and a 100 percent increase in FEP concentration. How-
ever, FEP levels were not different for group B and rural area residents.
Later surveys of children (Roels et al., 1980) were conducted in 1976, 1977 and 1978; the
former two in autumn, the latter in spring. In total there were five surveys conducted yearly
from 1974 to 1978. A group of age-matched controls from a rural area was studied each time
except 1977. In 1976 and 1978 an urban group of children was also studied.
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The overall age for the different groups ranged from 9 to 14 years (mean 11-12), The
length of residence varied from 0,5 to 14 years (mean 7-10 years). The subjects were always
recruited from the same five schools: one in the urban area, one in the rural area and three
in the swelter area (two <1 km and one, 2.5 km away). Air lead levels decreased from 1977 to
1578. However, the soil lead levels in the vicinity of the smelter were still elevated (<1
km, soil lead 2000-6000 pg/g). Oustfall lead in the area of the near schools averaged
16.4-22.0 mg/n?• day at 500 m from the stack, 5.8-7.2 sig/in2 • day at 700 m, about 2 mg/n^-day at
2
1000 m and fluctuating around 0.5-1 mg/m *day at 1.5 km and beyond. The particle size was
predominantly 2 pm in diameter with a secondary peak between 4 and 9 pm. The particle size
, * 4 JS
declined with increasing distance from the smelter (0.7-2.4 km).
In all, 661 children (328 boys and 333 girls) were studied over the years. Two hundred
fourteen children came from less than 1 km from the smelter, 169 children from 1.5 to 2.5 km
from the plant, 55 children lived in the urban area and 223 children lived in the rural area.
The air lead and blood lead results for the five, years are presented as Table 11-27. The
reported air leads are not calendar year averages. The table shows that blood lead levels
(electrothermal atomic absorption spectrophotometry) are lower in the girls than the boys.
Within 1 km of the smelter no consistent improvement in air lead levels was noted over the
years of the study. The mean blood leads for the children living at about 2.5 km from the
smelter never exceeded 20 pg/dl since 1975, although they were higher than for urban and rural
children.
The researchers then investigated the importance of the various sources of lead in
determining blood lead levels. Data were available from the 1976 survey on air, dust and hand
lead levels. Boys had higher hand dust lead than girls. Unfortunately, the regression analy-
ses performed on these data were based on the group means of four groups.
EPA has reanalyzed the 1976 study using original data provided by Dr. Roels on the 148
children. The air lead, playground dust lead, and hand lead concentrations were all highly
correlated with each other. The hand lead measurements are used here with due regard for
their limitations, because day-to-day variations in hand lead for individual children are
believed to be very large. However, even though repeated measurements were not available,
this is among the most usable quantitative evidence on the role of ingested hand dust in
childhood lead absorption.
Total lead content per hand is probably more directly related to ingested lead than is
the lead concentration in the hand dust. The linear regression model used above was fitted by
EPA using lead in air (Mg/m3), lead in hand dust (pg/hand), lead in playground dust (Mfl/fl) and
sex as covariates of blood lead. The lead variables were highly correlated, resulting in a
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TABLE 11-27. MEAN AIRBORNE AND BLOOD LEAD LEVELS RECORDED DURING FIVE DISTINCT SURVEYS
(1974 to 1978) FOR STUDY POPULATIONS OF 11-YEAR-OLD CHILDREN LIVING LESS THAN 1 to
OR 2.5 km FROM A LEAD SMELTER, OR LIVING IN A RURAL OR URBAN AREA
Blood lead concentration (gg/dl)
Study
populations
Pb-Air
(pg/m3)
total Population
n Mean i SO
n
Boys
Mean ± SO
n
Girls
Mean ± SD
1 Survey
<1 km
4.06
37
30.1 ±5.7
14
31.0
+
5.5
23
29.6
±
5.9
(1974)
2.5 km
1.00
—
—
14
21.1
±
3.4
—
—
Rural
0.29
92
9.4 i 2.1
28
9.7
±
1.6
64
9.3
±
2.2
2 Survey
<1 km
2.94
40
26.4 ± 7.3
19
27.4
±
6.5
21
25.4
~
8.1
(1975)
2.5 km
0.74
29
13.6 ± 3.3
17
14.8
+
3.6
12
11.9
±
1.9
Rural
0.31
45-
• 9.1 ± 3.1
14
8.2
±
2.1
31
9.5
t
3.4
3 Survey
<1 km
3.67
38
24.6 ± 8.7
18
28.7
±
8.0
20
20.8
±
7,6
(1976)
2.5 km
0.80
40
13.3 ± 4.4
24
15.6
+
2.9
16
9.8
±
3.8
Urban
0.45
26
10.4 ± 2.0
17
10.6
±
2.0
9
9,9
±
2.0
Rural
0.30
44
"9.0 ± 2.0
21
9.2
±
2.3
23
8.7
+
1.7
4 Survey
<1 km
3.42
56
28.9 ± 6.5
27
31.7
±
9.5
29
26.4
+
8.7
(1977)
2.5 km
0.49
50
14.8 ± 4.7
34
15.7
±
4.8
16
13.0
+
4.3
5 Survey
1 km
2.68
43
27.8 ± 9.3
20
29.3
9.8
23
26.5
±
8.9
(1978)
2.5 km
0.54
36
16.0 ± 3.8
26
16.6
±
3.5
10
14.3
+
4.2
Urban
0.56
29
12.7 i 3.1
18
13.4
+
2.3
11
11.5
+
4.0
Rural
0.37
42
10.7 ± 2.8
17
11.9
±
3.0
25
10.0
+
2.4
Source: Roels et al. 1980.
i,
statistically significant regression but not statistically significant coefficients. Thus the
playground dust measurement was dropped and the following model obtained with almost as small
a residual sum of squares,
In(Pb-Blood) = ln(7.37 + 2.46 Pb-Air + 0.0195 Pb-Hand + 2.10 Male)
(±.45) (±.58) (±.0062) (±0.56)
The fitted model for the 148 observations gave an R2 of 0.654 and a mean square error (Sa) of
0.0836 (GSO = 1.335). The significance of the estimated coefficient establishes that intake
of lead-bearing dust from the hands of children does play a role in childhood lead absorption
over and above the role that can be assigned to inhalation of air lead. Individual habits of
mouthing probably also affect lead absorption along this pathway. Note too that the estimated
inhalation slope, 2.46, is somewhat larger than most estimates for adults. However, the ef-
fect of ingestion of hand dust appears to be almost as large as the effect of air lead in-
halation in children of this age (9-14 years). Roels et al. (1980), using group means,
PB11A/B 11-67 7/29/83
-------
PRELIMINARY DRAFT
concluded that the quantitative contribution of hand lead to children's blood lead levels was
far greater than that of air lead.
The high mutual correlations among air, hand, and dust lead suggest the use of their
principal components or principal factors as predictors. Only the first principal component
(which accounted for 91% of the total variance in lead exposure) proved a statistically sig-
nificant covariate of blood lead. In this form the model could be expressed as
In(Pb-Blood) = ln(7.4Z + 1.56Pb-Air + 0.0120Pb-Hand + 0.00212Pb-Dust + 2.29 Hale)
The estimated standard error on the inhalation slope 1s ±0.47. The difference between these
Inhalation slope and hand lead coefficients 1s an example of the partial attribution of the
effects of measured lead exposure sources to those sources that are not measured.
11.4.1.9 Other Studies Relating Blood Lead Levels to Air Exposure. The following studies
also provide information on the relationship of blood lead to air lead exposures, although
they are less useful in accurately estimating the slope at lower exposure levels. The first
group of studies are population studies with less accurate estimates of Individual exposures.
The second group of studies represent Industrial exposures at very high air lead levels in
which the response of blood lead appears to be substantially different than at ambient air
levels.
The Tepper and Levin (1975) study included both air and blood lead measurements. House-
wives were recruited from locations in the vicinity of air monitors. Table 11-28 presents the
geometric mean air lead and adjusted geometric mean blood lead values for this study. These
values were calculated by Hasselblad and Nelson (1975). Geometric mean air lead values ranged
from 0.17 to 3.39 pg/m , and geometric mean blood lead values ranged from 12.7 to 20.1 Mfl/dl.
Nordman (1975) reported a population study from Finland in which data from five urban and
two rural areas were compared. Air lead data were collected by stationary samplers. All
levels were comparatively low, particularly 1n the rural environment, where a concentration of
0.025 MS/*3 was seen. Urban-suburban levels ranged from 0.43 to 1.32 jjg/m3.
A study was undertaken by Tsuchiya et al. (1975) in Tokyo using male policemen who
worked, but not necessarily lived, in the vicinity of air samplers. In this study, five zones
were established, based on degree of urbanization, ranging from central city to suburban. Air
monitors were established at various police stations within each zone. Air sampling was con-
ducted fro* September 1971 to September 1972; blood and urine samples were obtained from 2283
policemen in August and September 1971. Findings are presented in Table 11-29.
Goldsmith (1974) obtained data for elementary school (9- and 10-year-olds) and high
school students in 10 California communities. Lowest air lead exposures were 0.28 pg/m3 and
highest were 3.4 pg/m3. For boys 1n elementary school, blood lead levels ranged from 14.3 to
PB11A/B
11-68
7/29/83
-------
PRELIMINARY DRAFT
TABLE 11-28. GEOMETRIC MEAN AIR LEAD AND ADJUSTED BLOOO LEAD
LEVELS FOR 11 COMMUNITIES IN STUDY OF
TEPPER AND LEVIN (1975) AS REPORTED BY
HASSELBLAD AND NELSON (1975)
Age and smoking
Geometric mean
adjusted geometric
air lead,
mean blood lead,
Sample
Community
Mg/m3
Mg/d1
size
Los Alamos, NM
0.17
15.1
185
Okeana, OH
0.32
16.1
156
Houston, TX
0.85
12.7
186
Port Washington, NY
1.13
15.3
196
Ardmore, PA
1.15
17.9
148
Lombard, IL
1.18
14.0
204
Washington, DC
1.19
18.7
219
Philadelphia, PA
1.67
20.1
136
Bridgeport, IL
1.76
17.6
146
Greenwich Village, NY
2.08
16.5
139
Pasadena, CA
3.39
17.6
194
Multiple R2 = 0.240
Residual standard deviation = 0.262 (geometric standard deviation = 1.30)
TABLE 11-29. MEAN AIR AND BLOOD LEAD VALUES FOR
FIVE ZONES IN TOKYO STUDY
Air lead,
Blood lead,
Zones
Mg/m3
jjg/100 g
1
0.024
17.0
2
0.198
17.1
3
0.444
16.8
4
0.831
18.0
5
1.157
19.7
Source: Tsuchiya et al. 1975.
P811A/B
11-69
7/29/83
-------
PRELIMINARY ORAFT
23.3 M9/dl; those for girls ranged from 13.8 to 20.4 pg/dl for the same range of air lead ex-
posures. The high school student population was made up of only sales from some of the 10
towns. The air lead range was 0.77 to 2.75 jjg/m » and the blood lead range was 9.0 to 12.1
(jg/dl. The high school students with the highest blood lead levels did not come from the town
with the highest air lead value. However, a considerable lag time occurred between the col-
lection and analysis of the blood samples. In one of the communities the blood samples were
refrigerated rather than frozen.
Another California study (Johnson et al., 1975, 1976) examined blood lead levels in rela-
tion to exposure to automotive lead in two communities, Los Angeles and Lancaster (a city in
the high desert). Los Angeles residents studied were individuals living in the vicinity of
heavily traveled freeways within the city. They included groups of males and females, aged 1
through 16, 17 through 34, and 34 and over. The persons selected from Lancaster represented
similar age and sex distributions. On two consecutive days, blood, urine and fecal samples
were collected. Air samples were collected from one Hi-Vol sampler 1n Los Angeles, located
near a freeway, and two such samplers in Lancaster. The Los Angeles sampler collected for 7
days; the two in Lancaster operated for 14 days. Soil samples were collected in each area in
the vicinity of study subjects.
3
Lead in ambient air along the Los Angeles freeway averaged 6.3 t 0.7 pg/m and, in the
3
Lancaster area, the average was 0.6 ± 0.2 pg/« . The mean soil lead in Los Angeles was 3633
pg/g, whereas that found in Lancaster was 66.9 pg/g. Higher blood lead concentrations were
found in Los Angeles residents than in individuals living in the control area for all age
groups studied. Differences between Los Angeles and Lancaster groups were significant with
the sole exception of the older males. Snee (1981) has pointed out a disparity between blood
samples taken on consecutive days from the same child in the study. This calls into question
the validity of using this study to quantify the air lead to blood lead relationship.
Daines et al. (1972) studied black women living near a heavily traveled highway 1n New
Jersey. The subjects lived in houses on streets paralleling the highway at three distances:
3.7, 38.1 and 121.9 m. Air lead as well as blood lead levels were measured. Mean annual air
3
lead concentrations were 4.60, 2.41 and 2.24 pg/m , respectively, for the three distances.
The mean air lead concentration for the area closest to the' highway was significantly dif-
ferent from that in both the second and third, but the mean air lead concentration of the
third area was not significantly different from that of the second. The results of the blood
lead determinations paralleled those of the air lead. Mean blood lead levels of the three
groups of women, in order of increasing distance, were 23.1, 17.4 and 17.6 pg/dl, respec-
tively. Again, the first group showed a significantly higher mean than the other two, but the
second and third groups' blood lead levels were similar to each other. Daines et al. (1972),
in the same publication, reported a second study in which the distances from the highway were
33.5 and 457 meters and in which the subjects were white upper middle class women. The air
PB11A/B 11-70 7/29/83
-------
PRELIMINARY DRAFT
lead levels were trivially different at these two distances, and the blood lead levels did not
differ either. Because the residents nearest the road were already 33 m from the highway, the
differences in air lead may have been insufficient to be reflected in the blood lead levels.
{See Chapter 7)
A summary of linear relationships for other population studies has been extracted from
Snee (1981) and is shown in Table 11-30. The Fugas study is described later in Section
11.5,2.3. There is a large range of slope values (-0.1 to 3.1) with most studies in the range
of 1.0 to 2.0. Additional information on the more directly relevant studies is given in the
Summary Section 11.4.1.10.
TABLE 11-30. BLOOD lEAD-AIR LEAD SLOPES FOR SEVERAL POPULATION
STUDIES AS CALCULATED BY SNEE
Study
No,
Subjects
Sex
Slope
95% confidence
Intervals
Tepper & Levin
1935
Female
1.1
±1.8
(1975)
Johnson et al.
65
Male
0.8
±0.7
(1975)
96
Female
0.8
±0.6
Nordman (1975)
536
Male
1.2
±1.0
478
Female
0.6
±0.9
Tsuchiya et al.(1975)
537
Male
3.1
±2.2
Goldsmith (1974)
89
Male
-0.1
±0.7
79
Female
0.7
±0.7
fugas (1977)
352
Male
2.2
±0.7
Daines et al. (1972)
61
Female
(spring)
1.6
±1.7
Female (fall)
2.4
±1.2
Johnson et al.
37
Male
(1975)
(children)
1.4
±0.6
43
Female
(children)
1.1
±0.6
Goldsmith (1974)
486
Male & Female
(children)
2.0
±1.3
a0utlier results for four subjects deleted.
Source: Snee, 1981.
There is a great deal of information on blood lead responses to air lead exposures of
workers in lead-related occupations. Almost all such exposures are at air lead levels far in
excess of typical non-occupational exposures. The blood lead vs. air lead slope p is very
much smaller at high blood and air levels. Analyses of certain studies are shown in Table
11-31.
PB11A/B
11-71
7/29/83
-------
Study
Analyst (
TABLE 11-32. CROSS-SECTIOHAL OBSERVATIONAL STUOV WITH MEASURED INOIVIDUAL AIR LEAD EXPOSURE
R*
Model
Model
d.f.
Slope at an air l«g«l of
TToigTili3 2.0 M9/"3
Azar et <1. (1975)
Study done in
1970-1971 in five
U.S. cities, total
saaple size ¦ 149.
Blood loads ranged
fro» 8 to 40 pg/dl.
Air leads ranged
from 0.2 to 9.1
VU/m*
Azar at al. (1975) In (PBB) = 0.153 In (PBA) ~ separate Intercepts for each group
Snee (1982b)
1.019 H A 11A /BAA *
Ha—ond et al
(1981)
In (PBB) = 0.2669 In (P8A * separate background for each group)
~ 1,0842
(PB8)
= 0.179 (PSA ~ separate background for each group)
-0.098
0.502
0.497
0.49
2-57 1.43
(1.23, 3.91) (0.64, 2.30)
1.12 0.96
(0.29, 1.94) (0.25, 1.66)
1.08
1.07
EPA
In(PBB) = ln(l.318 PBA ~ separate background for each group)
0.491
6
1.32
1.32
9
(0.46, 2.17>
(0.46, 2.17)
IPA
In(PBB) « ln(2.902 PSA - 0.25? PBA ~ separate background
0.504
7
2.39
1.87
for each group)
EPA
In(PBB) = ln(l.342 PBA ~ separate background * age slope x age)
0.499
7
1.34
1.34
(0.32, 2.37)
(0.32 . 2.37)
EPA
ln(PB8) «= ln(1.593 PBA = comon intercept ~ age * separate age
0.489
7
1.59
1.59
slope)
(0.76, 2.42)
(0.76, 2.42)
EPA
ln(PB8) = tn(1.255 PBA ~ separate background ~ age ~ separate
0.521
11
1.26
1.26
age slope)
(0.46, 2.05)
(0.46, 2.OS)
EPA
In(PSB) « 0.2S ln-(PBA ~ separate background * age x separate
0.514
12
about 1.0
about 1.0
age slope)
(varies by
(varies by
city)
city)
:o
•<
Note: PBB stands for blood lead (|ig/d1); PBA stands for air lead (yg/*3); slope aeana^rate of change of blood lead per unit change in air lead at the
stated air lead value. The 95 percent confidence intervals for the slope are given in parentheses. These are approximate and should be used
with caution. The analyses labelled "EPA" are calculated from the original authors' data.
-------
TABLE 11-32. CROSS-SECT IOWU. OBSERVATIONAL STUDY WITH MEASURED INDIVIDUAL AIR LEAD EXPOSURE
Study
Analysis
Model
R*
"Model
d. f.
Slope at an air l»»d of
1.0jig/«3 2.0 Mq/«3
Azar at al. (1975)
Study don* In
1970-1971 in five
U.S. cities, total
saaple siie =* 149.
Blood leadi ranged
froa 8 to 40 MS/dl.
Air leads ranged
froa 0.2 to 9.1
jig/a3
Aaar et al. (197S)
In (P8B) - 0.153 In (PBA) * separate intercepts for each group
0.502
fi
2.57
1.43
(1.23, 3.91)
(0.64 , 2.30)
Snee (1962b)
In (P86) = 0.2669 In (PBA ~ separate background for each group)
0.497
7
1.12
0.96
~ 1.0842
(0.29, 1.94)
(0.25, 1.66)
Haaaond et al.
(P88)"1019 = 0.179 (PBA ~ separate background for each group)010*
0.49
8
1.08
1.07
(1981)
-0.098
EPA
In(PBfi) = )n(1.318 PBA ~ separate background for each group)
0.491
6
1.32
1.32
9
(0.46, 2.17)
(0.46, 2.17)
EPA
In(PBB) = 1(1(2.902 PBA - 0.257 PBA ~ separate background
0.504
7
2.39
1.87
for each group)
IPA
ln(P88) - ln(1.342 PSA * separate background * age slope x age)
0.499
7
1.34
1.34
(0.32, 2.37)
CO.32, 2.37)
EPA
1n(PB8) « ln(1.593 PBA ¦ coaaoo intercept ~ age x separate age
0.489
7
1.59
1.59
slope)
(0.76, 2,42)
(0.76, 2.42)
EPA
ln(PBB) - ln(1.2S5 PBA ~ separate background * age ~ separata
0.521
11
1.26
1.26
age slope)
(0.46, 2.05)
(0.46, 2.05)
EPA
ln(P8B) = 0.2S In-(PBA * separate background ~ age x separate
0.514
12
about 1.0
about 1.0
age slope)
(varies by
(varies by
city)
city)
3
Note: PBB stands for blood lead (|ig/dl); PBA stands for air lead (yg/as); slope aeanstrate of change of blood lead per unit change in air lead at the
stated air lead value. The 95 percent confidence intervals for the slope are given in parentheses. These are approxiaate and should be used
with caution. The analyses labelled "EPA" are calculated fro* the original authors' data.
-------
TASIE 11-33.
CROSS-SECTIONAL OBSERVATIONAL 5IUOIES OH CHILDREN WITH ESTIMATED AIR EXPOSURES
Study
Analysis
Node!
Model Slope at an air lead of
d.f. 1.0 no/.3 5.6 ugA.3
Kellogg Idaho/Silver
Valley study conducted
in 1974 based on about
880 children, Air
leads ranged fro*
0. S to 22 ng/«s.
Blood leads ranged
fro* 11 to 164
Yankel et al.
(1977)
Snee (1982c)
EPA
IPA
1n(P8B)
0.041 PBA ~ 2. 1x10 3 soil •» 0.087 dust
0.018 age ~ 0.024 occupation •» 3.14
Walter et
(1980)
ln(PBB) = 0.039 P8A ~ 0.065,ln (soil) ~ terms Jojf sex,
occupation, cleanliness, education, jjjca
ln(PBB) - ln(1.5? PBA to 0 0011 soil ~ term for sex,
occupation, cleanliness..education, pica)
In(PBS) = »1.(1.13 PBA ~ 0.026 PBA' ~ terms for soil, sex,
occupation, cleanliness, education, pica)
il. In(PBB) = separate slopes for air, dust, occupation, pica
sex and soil fay age
0.622
6
1.16
1.37
(1.09, 1.23)
(1.27, 1.46)
0-666
25
1.13
1.32
(1.06, 1.20)
(1 23, 1.42)
0.655
18
1.52
1.52
0.656
19
1.16
1.39
to 0.70
7
1.01 to 1.26
1.18 to 1.48
0.347
25
1.07
1.25
Kellogg Idaho/Silver Snee (1982a)
Valley study as above
restricted to 537 chil-
dren with air leads
below 10 m/w*
In(PBB) = 0.039 PBA ~ 0.055 In (soil) ~ term for sex, occupation
cleanliness, education, pica
(0.W, 1.25) (1.01, 1.S0)
Roels et al.
(1980)
Roels et al.
(1980) based
on 8 groups
EPA analysis
PBB * 0.007 PBA ~ 11.50 log(PB-Hand)
- 4.27
4.27
In(PBB) = ln(2.46 PBA ~ 0.0195 (Pb-Hand) ~ 2.1 (Male) ~ 7.37)
0.65
0.654
0.007
2.46
0.007
2.46
Angle and Hclntlr*
(1979)
Angle and
Nclntire (1979)
on 832 saaples
ages 6-18
ln(PB8) = In(S.l) + 0.03 In (PBA) ~ 0.10 In (PB-Soil)
~ 0.07 In (Pb-House Oust)
0.21
4
0.6
0.14
Angle et al.
(1983) on 1074
saaplts for ages
1-18
In(PBB) = ln(1.92 PflA ~ 0.00680 Pb-Soil
~ 0.00718 Pb-House Oust ~ 15.67)
0.199
4
1.9*
(0.74,3.10)
1.92
(0.74,3.10)
832 saaples ages
6 to 18
ln(PB8) = In (4.40 PBA to .00457 Pb-Soil
+ 0.00336 Pb-House Bust ~ 16.21)
0.262
4
4.40
(3.20.5.60)
4.40
(3.20.5.60)
Note: PBB stands for blood lead (pg/dl); PBA stands for air lead (tig/a3); slope neans rate of change of blood lead per unit change In air lead at the
stated air lead value. The 95 percent confidence intervals for the slope are given 1n parentheses. These are approximate and should be used
with caution. The analyses labelled "EPA" are calculated froa the original authors' data.
-------
TABLE 11-34. LONGITUDINAL EXPERIMENTAL STUDIES WITH MEASURED INDIVIDUAL AIR LEAD EXPOSURE
Experiment
Analysis
Model
Afr Lead
Blood Lead
Kctxw 1950-1971 Gross (1981) A PBB - 0.57 A PBA
1960-1969 Haaaond ei *1.(1981) A P88 = ^4 PSA, Pj by subject froa -0.6 to 2.94
SnM (1981) A PB8 = pjA PBA, p^ by subject fro* 0.4 to 2.4
EPA PBB ¦ PBA ~ background, p,j by subject froa -.34 to 2.60
0.6 to 36
0.6 to 9
ia to 4i
18 to 29
Ol
Griffin at al. KMlson at al.(1973) A P88 » 0.327 PSA * 3.236 * (2.10 PBA * 1.96) (In PBA ~ p^ by subject
1971-1972 Haaaond at al.(19Bl) A PBB = p A PBA, p - 1.90 at 3.2 and p = 1.54 at 10.9
Sitae (1961) A PBB * p^ A PBA, p^ by subject, p = 2.3 at 3.2 and p » 1.5 at 10.9
EPA A PBB = p.| A PBA, p, by subject, Man p - 1.52 at 3.2
and p = 1.77 at 10.9
0.15, 3.2
0.15, 10.9
11 to 32
14 to 43
o
30
>
Chaafcerlain at
al. 1973-1978
Chatfwrlatn et al.
(1978)
EPA
& PBB a p APBA, p '
A PBB - p APBA, p =
1.2 calculated
2.7 calculated
Rabtnowttz Sitae (1981)
at al. 1973-1974 £W
A PBB » p( APBA, P^ by subject froa 1.7 to 3,9
A PBB - p| APBA, p., by subject froa 1.59 to 3.56
0.2 to 2
14 to 28
-------
PRELIMINARY DRAFT
The blood lead inhalation slope estimates vary appreciably from one subject to another in
experimental and clinical studies, and from one study to another. The weighted slope and
standard error estimates from the Griffin study in Table 11-16 (1.75 ± 0.35) were combined
with those calculated similarly for the Rabinowitz study in Table 11-19 (2.14 ± 0.47) and the
Kehoe study in Table 11-20 (1.25 * 0.35 setting DH = 0), yielding a pooled weighted slope es-
3
timate of 1.64 ± 0.22 jag/dl per pg/m . There are some advantages in using these experimental
studies on adult males, but certain deficiencies need to be acknowledged. The Kehoe study ex-
posed subjects to a wide range of exposure levels while in the exposure chamber, but did not
control air lead exposures outside the chamber. The Griffin study provided reasonable control
of air lead exposure during the experiment, but difficulties in defining the non-inhalation
baseline for blood lead (especially in the important experiment at 3.2 pg/m > add much uncer-
tainty to the estimate. The Rabinowitz study controlled well for diet and other factors and
since they used stable lead isotope tracers, they had no baseline problem. However, the
actual air lead exposure of these subjects outside the metabolic ward was not well determined.
Among population studies, only the Azar study provides a slope estimate in which air lead
exposures are known for individuals. However, there was no control of dietary lead intake or
other factors that affect blood lead levels, and slope estimates assuming only air lead and
location as covariables (1.32 ± 0.38) are not significantly different from the pooled experi-
mental studies.
Snee and Pfeifer (1983) have extensively analyzed the observational studies, tested the
equivalence of slope estimates using pooled within-study and between-study variance com-
ponents, and estimated the common slope. The result of five population studies on adult males
(Azar, Johnson, Nordman, Tsuchiya, Fugas) was an inhalation slope estimate ±95 percent
confidence limits of 1.4 t 0.6. For six populations of adult females [Tepper-Levin, Johnson,
Nordman, Goldsmith, Daines (spring), Daines (fall)], the slope was 0.9 ± 0.4. For four
populations of children [Johnson (male), Johnson (female), Yankel, Goldsmith], the slope
estimate was 1.3 i 0.4, The between-study variance component was not significant for any
group so defined, and when these groups were pooled and combined with the Griffin subjects,
the slope estimate for all subjects was 1.2 t 0.2.
The Azar slope estimate was not combined with the experimental estimates because of the
lack of control on non-inhalation exposures. Similarly, the other population studies in Table
11-30 were not pooled because of the uncertainty about both inhalation and non-inhalation lead
exposures. These studies, as a group, have lower slope estimates than the individual experi-
mental studies.
There are no experimental inhalation studies on adult females or on children. The inha-
lation slope for women should be roughly the same as that for men, assuming proportionally
smaller air intake and blood volume. The assumption of proportional size is less plausible
PB11A/B 11-76 7/29/83
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PRELIMINARY DRAFT
for children. Slope estimates for children from population studies have been used in which
some other important covariates of lead absorption were controlled or measured, e.g., age,
sex, dust exposure in the environment or on the hands. Inhalation slopes were estimated for
the studies of Angle and Mclntire (1.92 ± 0.60), Roels (2.46 ± 0.58) and Yankel et al. (1.53 ±
0.064). The standard error of the Yankel study is extremely low and a weighted pooled slope
estimate for children would reflect essentially that study alone. In this case the small
standard error estimate is attributable to the very large range of air lead exposures of
3
children in the Silver Valley (up to 22 HS/m )• The relationship is in fact not linear, but
increases more rapidly in the upper range of air lead exposures. The slope estimate at lower
air lead concentrations may not wholly reflect uncertainty about the shape of the curve at
higher concentrations. The unweighted mean slope of the three studies and its standard error
estimate are 1.97 ± 0.39.
This estimate was not combined with the child population studies of Johnson or Goldsmith.
The Johnson study slope estimate used air lead measured at only two sites and is sensitive to
assumptions about data outliers (Snee, 1981), which adds a large non-statistical uncertainty
to the slope estimate. The Goldsmith slope estimate for children (2.0 ± 0.65) is close to
the estimate derived above, but was not used due to non-statistical uncertainties about blood
lead collection and storage.
One can summarize the situation briefly:
3
(1) The experimental studies at lower air lead levels, 3.2 pg/m or less, and lower
blood levels, typically 30 pg/dl or less, have linear blood lead inhalation
relationships with slopes g, of 0 to 3.6 for most subjects. A typical value of
1.64 ± 0.22 may be assumed for adults.
(2) Population cross-sectional studies at lower air lead and blood lead levels are
approximately linear with slopes p of 0.8 to 2.0.
\
(3) Cross-sectional studies ir^ occupational exposures in which air lead levels are
higher (much above,J.0 pg/m ) and blood lead levels are higher (above 40 Mg/dl),
show a much more shallow linear blood lead inhalation relation. The slope 0 is
in the range 0.03 to 0.2.
(4) Cross-sectional and experimental studies at levels of air lead somewhat above
the higher ambient exposures (9 to 36 pg/m ) and blood leads of 30 to 40 pg/dl
can be described either by a nonlinear relationship with decreasing slope or by
a linear relationship with intermediate slope, approximately p = 0.5. Several
biological mechanisms for these differences have been discussed (Hammond et
al., 1981; O'Flaherty et al., 1982; Chamberlain, 1983; Chamberlain and Heard,
1981). Since no explanation for the decrease in steepness of the blood lead
inhalation response to higher air lead levels has been generally accepted at
this time, there is little basis on which to select an interpolation formula
from low air lead to high air lead exposures. The increased steepness of the
inhalation curve for the Silver Valley/ Kellogg study is inconsistent with the
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other studies presented. It nay be that smelter situations are unique and nust
be analyzed differently, or it may be that the curvature is the result of
imprecise exposure estimates.
(5) The blood-lead inhalation slope for children is at least as steep as that for
adults, with an estimate of 1.97 ± 0.39 from three major studies (Yankel et
al., 1977; Roels, et al. (1980); Angle and Mclntire, 1979).
U.4.2 Dietary Lead Exposures Including Water
Another major pathway by which lead enters the body is by ingestion. As noted in Chap-
ters 6 and 7, the recycling of both natural and anthropogenic lead in the environment results
in a certain amount of lead being found in the food we eat and the water we drink. Both of
these environmental media provide external exposures to lead that ultimately increase internal
exposure levels in addition to Internal lead elevations caused by direct inhalation of lead in
air. The Nutrition Foundation Report (1982) presents a compilation of recent estimates of
dietary intakes in the United States and Canada. The report gives Information on relation-
ships between external lead exposures and blood lead levels. The mechanisms and absorption
rates for uptake of lead from food and water are described in Chapter 10. The purpose of the
present section is to establish (analogously to Section 11.4.1) the relationships between
external exposures to lead in food and drinking water and resulting internal lead exposures.
The establishment of these external and internal lead exposure relationships for the en-
vironmental media of food and water, however, is complicated by the inherent relationship be-
tween food and water. First, the largest component of food by weight is water. Second,
•drinking water is used for food preparation and, as shown in Section 7.3.1.3 provides addi-
tional quantities of lead that are appropriately included as part of external lead exposures
ascribed to food. Third, the quantity of liquid consumed daily by people varies greatly and
substitutions are made among different sources of liquid: soft drinks, coffee, tea, etc., and
drinking water. Therefore, at best, any values of water lead intake used in drinking water
calculations are somewhat problematic.
A further troubling fact is the influence of lead in the construction of plumbing facil-
ities. Studies discussed in Section 7.3.2.1.3 have pointed out the substantial lead exposures
in drinking water that can result from the use of lead pipes in the delivery of water to the
tap. This problem is thought to occur only in limited geographic areas in the U.S. However,
where the problem is present, substantial water lead exposures occur. In these areas one can-
not make a simplifying assumption that the lead concentration in the water component of food
1s similar to that of drinking water. But rather one is adding a potentially major additional
lead exposure to the equation.
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Studies that have attempted to relate blood lead levels to ingested lead exposures have
used three approaches to estimate the external lead exposures involved: duplicate meals, fe-
cal lead determinations, and market basket surveys. In duplicate diet studies, estimated lead
exposures are assessed by having subjects put aside a duplicate, of wjjatthpy eat at each meal
fcr a limited period of time. These studies probably provide a good, but short term, estimate
of the ingestion intake. However, the procedures available to analyze lead in foods have his-
torically been subject to inaccuracies. Hence, the total validity of data from this approach
has not been established. Studies relying on the use of fecal lead determinations face two
major difficulties. First, this procedure involves the use of a sathenatical estimate of the
overall absorption coefficient from the gut to estimate the external exposure. Until re-
cently, these estimates have not been well documented and were assumed to be relatively con-
stant. Sewer data discussed later show a much wider variability in the observed absorption
coefficients than was thought to be true. These new observations cloud the utility of studies
using this method to establish external/internal exposure relationships. Second, it is dif-
ficult to collect a representative sample.
The last approach is the market basket approach. This approach uses the observed lead
concentrations for a variety of food items coupled with estimated dietary consumption of the
particular food items. Some studies use national estimates of typical consumption patterns
upon which to base the estimated exposures. Other studies actually record the daily dietary
intakes. This approach faces similar analytic problems to those found in the duplicate diet
pproach. It also faces the problem of getting accurate estimates of dietary intakes. The
it ist current total diet study (Pennington, 1983) is described in Section 7.3.1.2.
Exposures to lead in the diet are thought to have decreased from the 1940's. Estimates
•om that period were in the range of 400-500 pg/day for U.S. populations. Current estimates
jr U.S. populations are under 100 pg/day for adults. Unfortunately, a good historical record
regarding the time course of dietary exposures is not available. In the years 1978-82, ef-
forts have been made by the American food canning industry in cooperation with the FDA to re-
duce the lead contamination of canned food. Data presented in Section 7.3.1.2.5 confirm the
success of this effort.
The specific studies available for review regarding dietary exposures will be organized
into three major divisions: lead ingestion from typical diets, lead ingestion from experi-
mental dietary supplements and inadvertent lead ingestion from lead plumbing.
11.4.2.1 Lead Ingestion from Typical Diets.
11.4.2.1.1 Ryu study on infants and toddlers. Ryu et al. (1983) reported a study of four
breast-fed infants and 25 formula-fed infants from 8 days to 196 days of age. After 112 days,
the formula-fed infants were separated into a group of 10 who received carton milk and a
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second group of seven who received either canned formula or heat-treated Bilk in cans. In ad-
dition to food concentrations, data were collected on air, dust and water lead. Hemoglobin
and FEP were also measured.
The trends in blood lead for the formula-fed infants are shown in Table 11-35. The re-
sults up to day 112 are averaged for all 25 infants. The estimated average intake was 17
pg/day for this time period. After day 112, the subgroup of seven infants fed either canned
formula or heat-treated cow's milk in cans (higher lead), had average estimated lead intake of
61 pg/day. This resulted in an increase of 7.2 pg/dl in the average blood lead for an in-
crease of 45 yg/day in leH^iltake. The estimated slope from this data is 0.16.
TABLE 11-35. BLOOD LEAD LEVELS AND LEAD INTAKE VALUES
FOR INFANTS IN THE STUDY OF RYU IT AL.
Age in Blood lead of combined Average lead intake of
Days group (ng/dl) combined group (uq/day)
8 8.9 17
28 5.8 17
55 5.1 17
84 5.4 17
112 6.1 17
Lower Lead Higher Lead Lower Lead Higher Lead
140 6.2 9.3 16 61
168 7.0 12.1 16 61
196 7.2 14.4 16 61
Source: Ryu et al. (1983).
11.4.2.1.2 Rabinowitz study. This study on male adults was described in Section 11.4.1 and
in Chapter 10, where ingestion experiments were analyzed 1n more detail (Rabinowitz et al.,
1980). As in other studies, the fraction of ingested stable isotope lead tracers absorbed
into the blood was much lower when lead was consumed with meals (10.3 ±2.2 percent) than
between meals (35 ± 13 percent). Lead nitrate, lead sulfide and lead cysteine as carriers
made little difference. The much higher absorption of lead on an empty stomach implies
greater significance of lead ingestion from leaded paint and from dust and soil when consumed
between meals, as seems likely to be true for children.
11.4.2.1.3 Hubermont study. Hubermont et al. (1978) conducted a study of pregnant women
living in rural Belgium because their drinking water was suspected of being lead contaminated.
This area was known to be relatively free of air pollution. Seventy pregnant women were
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recruited and were asked to complete a questionnaire. Information was obtained on lifetime
residence history, occupational history, smoking and drinking habits. First flush tap water
samples were collected from each home with the water lead level determined by fTameless atomic
absorption spectrophotometry. Biological samples for lead determination were taken at
delivery. A venipuncture blood sample was collected from the mother as was a fragment of the
placenta. An umbilical cord blood sample was used to estimate the newborn's blood lead
status.
For the entire population, first flush tap water samples ranged from 0.2 to 1228.5 Mg/1.
The mean was 109.4 while the median was 23.2. The influence of water lead on the blood lead
of the mother and infants was examined by categorizing the subjects on the basis of the lead
level of the water sample, below or above 50 pg/1. Table 11-36 presents the results of this
study. A significant difference in blood lead levels of mothers and newborns was found for
the water lead categories. Placenta lead levels also differed significantly between water
lead groups. The fitted regression equation of blood lead level for mothers is given in
summary Table 11-42.
11.4.2.1.4 Sherlock study. Sherlock et al. (1982) reported a study from Ayr, Scotland, which
considered both dietary and drinking water lead exposures for mothers and children living in
the area. In December 1980, water lead concentrations were determined from kettle water from
114 dwellings in which the mother and child lived less than 5 years. The adult women had
venous blood samples taken in early 1981 as part of a European Economic Community (EEC) survey
on blood lead levels. A duplicate diet survey was conducted on a random sample of these 114
women stratified by kettle water lead levels.
A study population of 11 mothers with infants less than 4 months of age agreed to
participate in the infant survey. A stratified sample of 31 of 47 adult volunteers was
selected to participate in the duplicate diet study.
Venous blood samples for adults were analyzed for lead immediately before the duplicate
diet study; in some instances additional samples were taken to give estimates of long term ex-
posure. Venous samples were taken from the infants immediately after the duplicate diet week.
Blood lead levels were determined by AAS with graphite furnace under good quality control.
Two other laboratories analyzed each sample by different methods. The data reported are based
on the average value of the three methods.
Dietary intakes for adults and children were quite different; adults had higher intakes
than children. Almost one third of the adults had intakes greater than 3 mg/week while only
20 percent of the infants had that level of intake. Maximum values were 11 mg/week for adults
and 6 mg/week for infants.
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The observed blood lead values in the dietary study had the following distributions:
>20 yg/dl "">30^g/dl >35 jjg/dl
Adults 55% -16% 2%
Infants 100% 55% 36%
EEC Directive 50% .10% 2%
TABLE 11-36. INFLUENCE OF LEVEL OF LEAD IN WATER
ON BLOOD LEAD LEVEL IN BLOOD AND PLACENTA
Comparison
Water
Mean
Median
Range
Significance
Group
Level
Low**
25.6
24
18-41
NS*
Age (Years)
High***
26.3
25
20-42
Pb-B mother
Low
10.6
9.9
5.1-21.6
<0.005
(Mg/dl>
High
13.8
13.1
5.3-26.3
Pb-B newborn
Low
8.8
8.5
3.4-24.9
<0.001
(pg/dl)
High
12.1
11.9
2.9-22.1
Pb placenta
Low
9.7
8.2
4.4-26.9
<0.005
(ng/100 g)
High
13.3
12.0
7.1-28
Water Pb
Low
11.8
6.3
0.2-43.4
(MQ/1)
High
247.4
176.8
61.5-1228.5
Source; Hubermont et al. (1978)
*NS means not significant
* "Water Lead <50 yig/1
***Water Lead >50 pg/1
Table 11-37 presents the crosstabulation of drinking water lead and blood lead level for
the 114 adult women in the study. A strong trend of Increasing blood lead levels with In-
creasing drinking water lead levels 1s apparent. A curvilinear regression function fits the
data better than a linear one. A similar model including weekly dietary intake was fitted to
the data for adults and infants. These models are in summary Tables 11-41 and 11-44.
The researchers also developed a linear model for the relationship between dietary Intake
and drinking water lead. The equation indicates that, when the concentration of lead in water
was about 100 vg/l, approximately equal amounts of lead would be contributed to the total
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TABLE
11-37.
BLOOD LEAD AND KETTLE WATER LEAD CONCENTRATIONS
FOR WOMEN LIVING IN AYR
Blood lead
MS per 100 ml
^ttter lead (pg/l)
<10
li-
as
100-
299
• 300-
499
500-
999
1000-
1499
>1500
Total
<10
11-15
16-20
21-25
26-30
31-35
36-40
>40
8
4
1
5
7
3
4
3
12
9
2
2
2
3
7
4
1
1
1
3
5
4
2
1
4
2
2
1
3
1
3
1
3
13
17
22
25
12
10
4
11
Total
13
19
28
19
19
8
8
114
week's intake from water arid from the diet; as water lead concentrations increase froi» this
value, the principal contributor would be water,
11.4.2.1.5 Central Directorate on Environmental Pollution study. The United Kingdom Central
Directorate on Environmental Pollution (1982) studied the relationship between blood lead
level and dietary and drinking water lead in infants. Subjects were first recruited by
soliciting participation of all pregnant women attending two hospitals and residing within a
single water distribution system. Each woman gave a blood sample and a kettle water sample.
The women were then allocated to one of six potential study groups based on the concentration
of water lead.
At the start of the second phase (duplicate diet) a total of 155 women volunteered
(roughly 17 to 32 per water lead level category). During the course of the study, 24 mothers
withdrew; thus a final study population of 131 mothers was achieved.
At 13 weeks of age, duplicate diet for a week's duration was obtained for each infant.
Great care was exerted to allow collection of the most accurate sample possible. Also, at
this time a variety of water samples were collected for subsequent lead analysis.
Blood samples were collected by venipuncture fro* mothers before birth, at delivery, and
about the time of the duplicate diet. A specimen was also collected by venipuncture from the
infant at the time of the duplicate diet. The blood samples were analyzed for lead by graph-
ite furnace AAS with deuterium background correction. Breast milk was analyzed analogously to
the blood sample after pretreatment for the different matrix. Water samples were analyzed by
flame atomic absorption. Food samples were analyzed after ashing by flameless atomic absorp-
tion.
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loth Mothers and infants exhibited increased lead absorption by EEC directive standards.
The infants generally had higher blood leads than the mothers. However, in neither population
was there evidence of substantial lead absorption.
Water lead samples ranged from less than 50 pg/1 to greater than 500 pg/1» which was ex-
pected due to the sampling procedure used. First draw samples tended to be higher than the
other samples. The composite kettle samples and the random daytime samples taken during the
duplicate diet week were reasonably similar: 59 percent of the composite kettle samples con-
tained up to 150 Hfl/1 as did 66 percent of the random daytime samples.
lead intakes from breast milk were lower than from duplicate diets. The lead intakes
estimated by duplicate diet analysis ranged from 0.04 mg/week to 3.4 mg/week; about 1/4 of the
diets had intakes less than 1.0 mg/week. The minimum intakes were truncated, as the limit of
detection for lead was 10 MQ/^g and the most common diets weighed 4 kg or more.
The authors used both linear and cube root models to describe their data. Models rela-
ting blood lead levels of infants to dietary intake are in Table 11-41. Models relating blood
lead levels for both mothers and infants to first flush water lead levels and running water
lead levels are in Tables 11-43 and 11-44, respectively. In most cases, the nonlinear (cubic)
model provided the best fit. Figure 11-15 illustrates the fit for the two models showing
infant blood lead levels vs. dietary lead intake.
11.4.2.1.6 Pocock study. Pocock et al. (1983) have recently reported an important study ex-
amining the relationship in middle aged men of blood lead level and water lead levels. Men
aged 40 to 59 were randomly selected from the registers of general practices located in 24
British towns. Data were obtained between January 1978 and June 1980.
Blood lead levels were obtained on 95 percent of the 7378 men originally selected. The
levels were determined by microatomic absorption spectrophotometry. A strict internal and ex-
ternal quality control program was maintained on the blood lead determinations for the entire
study period. Tap water samples were obtained on a small subset of the population. About 40
men were chosen in each of the 24 towns to participate in the water study. First draw samples
were collected by the subjects themselves, while a grab daytime and flushed sample were col-
lected by study personnel. These samples were analyzed by several methods of AAS depending
on the concentration range of the samples.
Blood lead and water lead levels were available for a total of 910 men from 24 towns.
Table 11-38 displays the association between blood lead levels and water lead levels. Blood
lead levels nearly doubled from the lowest to highest water lead category.
The investigators analyzed their data further by examining the form of the relationship
between blood and water lead. This was done by categorizing the water lead levels into nine
intervals of first draw levels. The first group (<6 m9/') tad 473 men while the remaining
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LINEAR
EQUATION
CUBE ROOT
EQUATION
E
8
r»
3
• •
o
o
3
• ••
a
«e
• •
0
1-0
LEAD INTAKE, mg/wk
Figure 11-15. Blood-lead concentrations versus weekly lead
intake for bottle-fed Infants.
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TABLE 11-38. RELATIONSHIP OF BLOOD LEAD (pg/dl)
AND WATER LEAD (|jfl/dl) IN 910 MEN AGED 40-59 FROM 24 BRITISH TOWNS
First Draw
Water Lead
(Mfl/1)
Number of
Men
Mean Blood
Lead
(Mg/dl)
Standard
Deviation
% with
Blood Lead
>35 Mg/dl
<50
789
15.06
5.53
0.7
50-99
69
18.90
7.31
4.3
100-299
40
21.65
7.83
7.5
£300
12
34.19
15.27
41.7
Total
910
15.89
6.57
1.9
Daytime
Water Lead
(M8/1)
<50
845
• 15.31
5.64
0.7
50-99
36
19.62
7.89
8.3
100-299
23
24.78 v
%
9.68
17.4
2300
5
39.78
15.87
60.0
Total
909
15.85
6.44
1.8
Source: Pocock et al. (1983).
eight intervals had 50 men each. Figure 11-16 presents the results of this analysis. "The
impression is that mean blood lead increases linearly with first draw water lead except for
the last group with very high water concentrations." The regression line shown in the figure
is only for men less than 100 and is given in Table 11-43. A separate regression was
done for the 49 men whose water lead exposures were greater than 100 jjg/1. The slope for the
second line was only 23 percent of the first line.
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Additional analyses were done examining the possible influence of water hardness on blood
lead levels, A strong negative relationship (r = -0.67) was found between blood lead level
and water hardness. There is a possibility that the relationship between blood lead and water
hardness was due to the relationship of water hardness and water lead. It was found that a
relationship with blood lead and water hardness still existed after controlling for water lead
level.
The authors come to the following- conclusion regarding the slope of the relationship
between blood lead and water lead:
This study confirms that the relation is not linear at higher levels. Previous
research had suggested a power function relationship—for example, blood lead in-
creases as the cube root of water lead. Our data, based on a large and more
representative sample of men, do not agree with such a curve, particularly at low
concentrations of water lead.
1.25
1.2
©.7 h-
0t
0
SO
100
320 360
FIRST DRAW WATER LEAD i^g/U
I Mil I i
ei 62
473 60 61 50 65 43 49
49
Figure 11-16. Mean blood lead for men grouped by first draw water concentra-
tion.
Source: Pocock et al. (1983).
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11.4.2.2. Lead Ingestion from Experimental Dietary Supplements.
11.4.2.2.1 Kehoe study. Experimental studies have been used to study the relationship of
food lead and blood lead levels. Gross (1981) reanalyzed the results of Kehoe. Oral doses of
lead Included 300, 1000, 2000, and 3000 Mfl/day. Each subject had a control period and an ex-
posure period. Some also had a post-exposure period. Blood samples were collected by veni-
puncture and analyzed by spectrograph!c and dithlzone methods during the study years. The
ingestion doses were in addition to the regular ingestion of lead from the diet. The results
of the dose response analysis for blood lead concentrations are summarized in Table 11-39.
Both subjects MR and EB had long exposure periods, during which time their blood lead
levels increased to equilibrium averages of 53 and 60 pg/dl, respectively. The exposure for
IF was terminated early before his blood lead had achieved equilibrium. No response 1n blood
lead was seen for subject SW whose supplement was 300 pg/day.
TABLE 11-39. DOSE RESPONSE ANALYSIS FOR BLOOD LEAD LEVELS IN THE KEHOE STUDY
AS ANALYZED BY GROSS (1981)
Difference from control
Added lead
Diet
Feces
Urine
Blood
Subject
(Mg/day)
(Mg/day)
(Mg/day)
(Mg/day)
(pg/dl)
SW
300
308
208
3
-l
MR
1000
1072
984
55
17
EB
2000
1848
1547
80
33
IF*
3000
2981
2581
49
19
"Subject did not reach equilibrium.
11.4.2.2.2 Stuik study. Stuik (1974) administered lead acetate in two dose levels (20 and 30
pg/kg body weight-day) to volunteers. The study was conducted in two phases. The first
phase was conducted for 21 days during February-March 1973. Five males and five females aged
2+
18-26 were exposed to a daily dose of 20 /kg of body weight. Five males served as
2+
controls. In the second phase, five females received 20 |ig Pb /kg body weight and five males
2+
received 30 pg Pb /kg body weight. Five females served as controls. Pre-exposure values
were established during the week preceding the exposures in both phases. Blood lead levels
were determined by HesseVs method.
The results of phase I for blood lead levels are presented in Figure 11-17. Blood lead
levels appeared to achieve an equilibrium after 17 days of exposure. Male blood lead levels
went from 20.6 pg/g to 40.9 jjg/fl while females went from 12.7 to 30.4 pg/g. The males seemed
to respond more to the same body weight dose.
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BOO
Tl TT
> CONTROL QROUP
¦ EXPOSED MALE SUBJECTS: 20 ^/kg(day
> EXPOSED FEMALE SUBJECTS: 20 pgfko'day
900
100
, — *
/
• Pb EXPOSURE-
J L
C» EPTA
• MALE QROUP
-L_l
C.EPTA_
FEMALE QROUP
1 3 8 10 16 17 22 29 31
DAYS
Figure 11-17. Average PbB levels, Exp. I.
Source: Stuik (1974).
38
48
i i—i—r
600
CONTROL QROUP
EXPOSED MALE SUBJECTS: 30 ugikgfday
EXPOSED FEMALE SUBJECTS: 20 HS'kB'day
V s
• Pb EXPOSURE*
I I I
C» EPTA
MALE GROUP |
P011B/A
*2 0 4 7 11 14 18 21 26 27
DAYS
Figure 11-18. Average PbB levels. Exp. II.
Source: Stuik (1974).
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In phase II, males were exposed to a higher lead dose (30 pg/kg-day). Figure 11-19 dis-
plays these results. Male blood lead rose higher than 1n the first study (46.2 vs. 40.9
M9/s); furthermore, there was no indication of a leveling off. Females also achieved a higher
blood lead level (41.3 vs. 30.4), which the author could not explain. The pre-exposure level,
however, was higher.for the second phase than the first phase (12.7 vs. 17,3 pg/g).
11.4.2.2.3 Cools study. Cools et al. (1976) extended the research of Stuik (1974) by ran-
domly assigning 21 male subjects to two groups. The experimental group was to receive a 30
pg/kg body weight dose of oral lead acetate long enough to achieve a blood lead level of 30.0
pg/g, when the lead dose would be adjusted downward to attempt to maintain the subjects at a
blood lead level of 40.0 pg/g. The other group received a placebo.
In the pre-exposure phase, blood lead levels were measured three times, while during ex-
posure they were measured once a week, except for the first three weeks when they were deter-
mined twice a week. Blood lead was measured by flame AAS according to the Westerlund modifi-
cation of Hessel's method.
Pre-exposure blood lead values for the 21 volunteers averaged 172 ppb. The effect of
ingestion of lead acetate on blood lead is displayed in Figure 11-19. After 7 days mean blood
lead levels had increased from 17.2 to 26.2 pg/g. The time to reach a blood lead level of
35.0 pg/g took 15 days on the average (range 7-40 days).
11.4.2.2.4 Schleqel study. Schleqel and Kufner (1979) report an experiment in which two sub-
+2
jects received daily oral doses of 5 mg Pb as an aqueous solution of lead nitrate for 6 and
13 weeks, respectively. Blood and urine samples were taken. Blood lead uptake (from 16 to 60
pg/dl in 6 weeks) and washout were rapid in subject HS, but less so in subject GK (from 12 to
29 pg/dl in 6 weeks). Time series data on other heme system indicators (FEP, 6-ALA-O,
6-ALA-U, coproporphyrin III) were also reported.
11.4.2.2.5 Chamberlain study. This study (Chamberlain et al., 1978) was described in Section
11.4.1, and in Chapter 10. The ingestion studies on six subjects showed that the gut absorp-
tion of lead was much higher when lead was ingested between meals. There were also dif-
ferences in absorption of lead chloride and lead sulfide.
11.4.2.3 Inadvertent lead Ingestion from Lead Plumbing.
11.4.2.3.1 Early studies. Although the use of lead piping has been largely prohibited in
recent construction, occasional episodes of poisoning from this lead source still occur.
These cases most frequently involve isolated farms or houses in rural areas, but a surprising
urban episode was revealed in 1972 when Beattie et al. (1972a,b) showed the seriousness of the
situation in Glasgow, Scotland, which had very pure but soft drinking water as its source.
The researchers demonstrated a clear association between blood lead levels and inhibition of
the enzyme ALA-D in children living in houses with (1) lead water pipes and lead water tanks,
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PRELIMINARY DRAFT
450
PREEXPOSURE
EXPOSURE
400
360
JQ
&
* 300
m
i
# EXPOSED
-------
PRELIMINARY DRAFT
(2) no lead water tank but with more than 60 ft of lead piping and (3) less than 60 ft of lead
piping. The mean lead content of the water as supplied by the reservoir was 17.9 pg/1; those
taken from the faucets of groups 1, 2 and 3 were 934, 239 and 108 pg/l» respectively.
Another English study (Crawford and Crawford, 1969) showed a clear difference between the
bone lead contents of the populations of Glasgow and London, the latter having a hard, nonsol-
vent water supply.
In a study of 1200 blood donors in Belgium (DeGraeve et al., 1975), persons from homes
with lead piping and supplied with corrosive water had significantly higher blood lead levels.
11.4.2.3.2 Hoore studies. H. R. Moore and colleagues have reported on several studies rela-
ting blood lead levels to water lead levels. Hoore (1977) studied the relationship between
blood lead level and drinking water lead in residents of a Glasgow tenement. The tenement was
supplied with water from a lead-lined water tank carried by lead piping. Water samples were
collected during the day. Comparative water samples were collected from houses with copper
pipes and from 15 lead plumbed houses. Blood samples were taken wherever possible from all
inhabitants of these houses. The data indicated that if a house has lead lined pipes, it is
almost impossible to reach the WHO standard for lead in water. Linear regression equations
relating blood lead levels to first flush and running water lead levels are in Tables 11-43
and 11-44.
Moore et al. (1977) also reported the analysis of blood lead and water lead data col-
lected over a four year period for different sectors of the Scottish population. The combined
data showed consistent increases In blood lead levels as a function of first draw water lead,
but the equation was nonlinear at the higher range. The water lead values were as high as
2000 jjg/1. The fitted regression equation for the 949 subjects is 1n Table 11-43.
Moore et al. (1981a,b) reported a study of the effectiveness of control measures for
plumbosolvent water supplies. In autumn and winter of 1977, they studied 236 mothers aged 17
to 37 in a post-natal ward of a hospital in Glasgow with no historical occupational exposure.
Blood lead and tap water samples from the home were analyzed for lead by AAS under a quality
control program.
A skewed distribution of blood lead levels was obtained with a median value of 16.6
pg/dl; 3 percent of the values exceeding 41 yg/dl. The geometric mean was 14.5 pg/dl. *
curvilinear relationship between blood lead level and water lead level was found. The log of
the maternal blood lead varied as the cube root of both first flush and running water lead
concentrations. In Moore et al. (1979) further details regarding this relationship are
provided. Figure 11-20 presents the observed relationship between blood lead and water lead.
In April 1978 a closed loop lime dosing system was installed. The pH of the water was
raised from 6.3 to 7.8. Before the treatment, more than 50 percent of random daytime water
samples exceeded 100 pg of Pb/1, the WHO standard. After the treatment was implemented, 80
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PRELIMINARY DRAFT
3 4 6
23.6 „ WATER LEAD, jiM
28
24 26 2B 24 23 N0 |N
UP TO IOmM GROUP
Figure 11-20. Cube root regression of blood lead on first flush water lead.
This shows mean ± S.D, of blood lead for pregnant women grouped in 7
intervals of first flush water lead.
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PRELIMINARY DRAFT
percent of random samples were less than 100 pg/1. It was found, however, that the higher pH
was not maintained throughout the distribution system. Therefore, in August 1980, the pH was
raised to 9 at the source, thereby maintaining the tap water at 8. At this time more than 95
percent of random daytime samples were less than 100 (jg/1.
In the autumn and winter of 1980, 475 mothers from the same hospital were studied. The
median blood lead was 6.6 pg/dl and the geometric mean was 8.1 pg/dl. Comparison of the fre-
quency distributions of blood lead between these two blood samplings show a remarkable drop.
No other source of lead was thought to account for the observed change.
11.4.2.3.3 Thomas study. Thomas et al. (1979) studied women and children residing on two
adjacent housing estates. One estate was serviced by lead pipes for plumbing while the other
was serviced by copper pipe. In five of the homes in the lead pipe estate, the lead pipe had
been replaced with copper pipe. The source water is soft, acidic and lead-free.
Water samples were collected from the cold tap in the kitchen in each house on three oc-
casions at two-week intervals. The following water samples were collected: daytime - first
water out of tap at time of visit; running - collected after tap ran moderately for 5 minutes
after the daytime sample; and first flush - first water out of tap in morning (collected by
residents). Lead was analyzed by a method (unspecified in report) that was reportedly under
quality control.
Blood samples were collected from adult females (2.5 ml venipuncture) who spent most of
the time in the home and from the youngest child (capillary sample). Blood samples were ana-
lyzed for lead by a quality controlled unspecified method. Blood lead levels were higher in
the residents of the lead estate homes than in the residents of the copper estate homes.
Median levels for adult females were 39 pg/dl and 14.5 pg/dl for the lead and copper estate
homes, respectively. Likewise, children's blood lead levels were 37 pg/dl and 16.6 pg/dl,
respectively. Water lead levels were substantially higher for the lead estate than for the
copper estate. This was true for all three water samples.
The researchers then monitored the effectiveness of replacing the lead pipe on reducing
both exposure to lead in drinking water and ultimately blood lead levels. This monitoring was
done by examining subsamples of adult females for up to 9 months after the change was
implemented. Water lead levels became indistinguishable from those found in the copper estate
homes. Blood lead levels declined about 30 percent after 3 to 4 months and 50 percent at 6
and 9 months. At 6 months the blood lead levels reached those of women living in the copper
estates. A small subgroup of copper estate females was also followed during this time. No
decline was noted among them. Therefore, it was very likely that the observed reduction in
blood lead levels among the other women was due to the changed piping.
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PRELIMINARY DRAFT
The researchers then analyzed the form of the relationship between blood lead levels and
water lead levels. They tried several different shapes for the regression line. Curvilinear
models provided better fits. Figure 11-21 depicts the scatter diagram of blood lead and water
lead. An EPA analysis of the data is in Table 11-43.
A later publication by Thomas (1980) extended his earlier analysis. This more extensive
analysis was limited to lead estate residents. Subjects who did not consume the first drawn
water from the tap had significantly lower blood lead levels than those who did (10.4 pg/dl
difference). No gradient was noted in blood lead levels with increasing water consumption.
Furthermore, no gradient in blood lead levels was noted with total beverage consumption (tea
ingestion frequency).
11.4.2.3.4 Worth study. In Boston, Massachusetts an investigation was made of water distri-
bution via lead pipes. In addition to the data on lead in water, account was taken of socio-
economic and demographic factors as well as other sources of lead in the environment (Worth et
al., 1981). Participants, 771 persons from 383 households, were classified into age groups of
less than 6, 6 to 20, and greater than 20 years of age for analysis. A clear association
between water lead and blood lead was apparent (Table 11-40). For children under 6 years of
age, 34.6 percent of those consuming water with lead above the U.S. standard of 50 pg/1 had a
blood lead value greater than or equal to 35 HSJ/dl, whereas only 17.4 percent of those con-
suming water within the standard had blood lead values of greatwstlfafl or equal to 35 pg/dl.
Worth et al. (1981) have published an extensive regression analysis of these data. Blood
lead levels were found to be significantly related to age, education of head of household, sex
and water lead exposure. Of the two types of water samples taken, standing grab sample and
running grab sample, the former was shown to be more closely related to blood lead levels than
the latter. Regression equations are given in Tables 11-43 and 11-44. .
11.4.2.4 Summary of Dietary Lead Exposures Including Water. It is difficult to obtain accu-
rate dose-response relationships between blood lead levels and lead levels in food or water.
Dietary intake must be estimated by duplicate diets or fecal lead determinations. Water lead
levels can be determined with some accuracy, but the varying amounts of water consumed by dif-
ferent individuals adds to the uncertainty of the estimated relationships.
Studies relating blood lead levels to dietary lead intake are compared in Table 11-41.
Most of the subjects in the Sherlock et al. (1982) and United Kingdom Central Directorate on
Environmental Pollution (1982) studies received quite high dietary lead levels (>300 Mfl/day).
The fitted cubic equations give high slopes at lower dietary lead levels. On the other hand,
the linear slope of the United Kingdom Central Directorate on Environmental Pollution (1982)
study is probably an underestimate of the slope at lower dietary lead levels. For these
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PRELIMINARY DRAFT
MAXIMUM WATER LEAD
LEVELS ON COPPER' ESTATE
MEDIAN WATER LEAD
LEVELS ON 'LEAD' ESTATE
FIRST FLUSH WATER LEAD. mg/IKw
Figure 11-21. Relation of blood lead (adult femala) to first flush water lead In
combined estates. (Numbers are coincidental points.* 9 - S or more.) Curve a,
present data; curve b, data of Moore eta/.
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PRELIMINARY DRAFT
TABLE 11-40. BLOOD LEAD LEVELS OF 771 PERSONS IN RELATION
TO LEAD CONTENT OF DRINKING WATER, BOSTON, MA
Persons consuming water (standing grab samples)
<50
Mfl n>/i
in
All1
ua Pb/1
Blood lead
levels, pg/dl
No.
Percent
No.
Percent
Total
<35
622
91
68
77.3
690
>35
61
9
20
22.7
81
Total
683
100
88
100.0
771
X2 * 14.35; df = 1.
P <0.01.
Source: Worth et al. (1981).
reasons, the Ryu et al. (1983) study is the most believable, although it only applies to in-
fants. Estimates for adults should be taken from the experimental studies or calculated from
assumed absorption and half-life values.
The experimental studies are summarized in Table 11-42. Most of the dietary intake sup-
plements were so high that many of the subjects had blood lead concentrations much in excess
of 30 jjg/dl for a considerable part of the experiment. Blood lead levels thus may not
completely reflect lead exposure, due to the previously noted nonlinearity of blood lead re-
sponse at high exposures. The slope estimates for adult dietary intake are about 0.02 pg/dl
increase in blood lead per pg/day intake, but consideration of blood lead kinetics may in-
crease this value greatly. Such values are a bit lower than those estimated from the popu-
lation studies extrapolated to typical dietary intakes in Table 11-41, about 0.05 yg/dl per
Mfl/day. The value for infants is much larger.
The studies relating first flush and running water lead levels to blood lead levels are
in Tables 11-43 and 11-44, respectively. Many of the authors chose to fit cube root models to
their data, although polynomial and logarithmic models were also used. Unfortunately, the
form of the model greatly influences the estimated contributions to blood lead levels from
relatively low water lead concentrations.
The models producing high estimated contributions are the cube root models and the loga-
rithmic models. These models have a slope that approaches infinity as water lead concentra-
tions approache zero. All other are polynomial models, either linear, quadratic or cubic.
The slopes of these models tend to be relatively constant at the origin.
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TABLE 11-41. STUDIES RELATING BLOOO LEAO LEVELS (|
-------
TABLE 11-42. STUDIES INVOLVING BLOOO IEAO LEVELS (vq/4\)
At® EXPERIMENTAL DIETARY INTAKES
Study
Subjects
Exposure
Font of Lead
Blood lead
Initial
Final
Slope* pg/dl
per pg/d.
Stuik (1974)
5 adult aale students
20 Mg Pb/kg/day - 21 d.
Lead acetate
20.6
40.9
0.01?**,***
Study 1
S adult female students
20 pg Pb/kg/day - 21 d.
Lead acetate
12.7
30.4
0.018**,***
5 adult aale students
Controls - 21 d.
Placebo
20.6
18.4
-
3D
Study II
5 adult feaale students
20 pg Pb/kg/day
Lead acetate
17.3
41.3
0.022
!—
5 adult male students
30 h9 Pb/kg/day
Lead acetate
16.1
46.2
0.014
X
5 adult feaale students
Controls
Placebo
-17.0
-17.0
-
Cools et al.
11 adult aates
30 pg Pb/kg/day -7 days
Lead acetate
17.2
26.2
0.027***
3D
«<
(1976)
10 -Huit Bales
Controls
Placebo
-19.0
-
O
Schlegel and
1 adult aale
50 tig Pb/kg/day - 6 *k.
Lead nitrate
16.5
64.0
0.014
TO
>
Kufner (1979)
1 adult aale
70 pg Pb/kg/day -13 wk.
Lead nitrate
12.4
30.4
0.004****
Gross (1979)
1 adult aale
300 tig/day
Lead acetate
-1
[0]
analysis of
1 adult.aale
1000 (ig/itey
Lead acetate
~17
0.017
Kehoe's
1 adult aale
2000 pg/day
Lead acetate
~33
0.016
experiaents
1 adult aale
MOO pg/day
Lead acetate
~19
0.006*****
* Exposure (pg/d) « Exposure (pg/kg/day) x 70 kg for Males, 55 kg for females. Slope = (Final - Initial Blood Lead)/Exposure (pg/d).
** Corrected for decrease of 2,2 pg/dl in control Mies.
*** Assumed mean life 40d. This increases slope estisate for short-tera studies. Stufk Study I would be 0.042, 0.044 respectively for Mies, feaales.
**** Assumed liaited absorption of lead.
***** Removed froa exposure before equilibrium.
-------
TABLE 11-43. STUOIES RELATING BLOOO IEAO LEVELS (yg/dl) TO FIR5T-FLUSM WATER LEAD (Mfl/1)
Estimated
Predicted blood lead
Blood
contribution (pg/dl
for
Model
lead at
a given water lead (pg/1)
Study
Analysis
Model
R*
D.F.
0 HjO Pb
5
10
25
50
North ct <1. (1981) study of 524
Worth et al. (1981)
In (P68) = 2.729 PBW - 4.699 (P6W)1 ~
0.18
14
20.5
0.3
0.6
1.4
2.7
subjacts in greater Boston. Water
2.116 (PBW)* + other teras for age,
leads (standing water) ranged froa
sex, education, dust (P6W is in ag/1)
<13 to 1108 fg/l. Blood leads
ranged froa 6 to 71.
EPA
ln(PB8) = In (40.69 PBW - 21.89 (P8W)2
0.18
11
21.1
0.2
0.4
1.0
2.1
~ other teras for age, sex, education,
dust) (PBW is in ag/1)
Moore et al. (1979) study of 949
Noore et al. (1979)
PBB = 11.0 ~ 2.36 (PBW)173
2
11.0
4.0
5.1
8.9
8.7
subjects froa different areas of
Scotland. Water leads were as
high as 2000 iig/1.
Hubemont et *1. (1978) study of
Huberaont et al.
PBB = 9.62 ~ 0.756 In (PBW)
0.14
2
8.4*
2.4
3.0
3.7
4.2
70 pregnant woaen in rural Belgiua.
(1978)
Water leads ranged froa 0.2 to
1228.5 Mfl/1. Blood leads ranged
froa 5.1 to 26.3 moAII.
U.K. Central Directorate (1982)
U.K. Central
PBB = 13.2 ~ 1.8 (P8W)173
0.11
2
13.2
3.1
3.9
5.3
6.6
study of 128 aotbers in greater
Directorate on
PBB = 18.0 ~ 0.069 PBW ;r
0.05
2
18.0
0.0
0.1
0.2
0.4
Glasgow, Water leads ranged froa
Environaental
under SO \>qt\ (35X) to over 500
Pollution
Mfl/1 (11X). Blood leads ranged
(1982)
froa under 5 |ig/dl (ZX) to over
35 f«/dl (5%).
U.K. Central Directorate (1982)
U.K. Central
PBB = 9.4 * 2.4 (PBW)1/3
0.17
2
9.4
4.1
5.2
7.0
8.8
study of 126 infants (as above).
Directorate on
PBB = 17,1 ~ 0.018 PBW
0.12
2
17.1
0.1
0.2
0.4
0.9
Blood leads ranged froa under 5
Environaental
jig/dl (4%) to over 40 yg/dl (4%).
Pollution
(1982)
Thoaas et al. (1979) study of 115
EPA
In (PBB) = [14.9 ~ 0.041 PBW - 0.000012
0.61
3
14.9
0.2
0.4
1.0
2.0
adult Welsh fenales. Water leads
(PBW)*]
ranged froa <10 to 2800 pg/dt.
Blood leads ranged froa 5 to 85
(jg/dl.
Noore (1977) study of 75 residents
Noore (1977)
PBB = 15.7 ~ 0.015 PBW
0.34
2
15.7
0.1
0.2
0.4
0.8
of a Glasgow teneaent
Pocock et al. (1983) study of 7735
Pocock et al. (1983)
PBB = 14.48 ~ 0.062 PBW
2
14.5
0.3
0.6
1.6
3.1
¦en aged 40-59 in Great Britain.
Water leads restricted to <100 yg/1.
*ainiaua Mt«r lead of 0.2 pg/dl used instead of 0.
-------
TABLE 11-44. STUDIES RELATING BtOOO IE AO lEVEtS (|ig/)
Model
Estimated Predicted blood lead
Stood contribution (|>g/d1) for
lead at a given water lead (pg/1)
Study
Analysis
Mode!
9*
O.F.
0 H20 Pb
5
10
2b
M
Worth «t al. (1981) study of SZ4 sub-
tPA
In (PBS) = (0.0425 PBW ~ other tents for
0.153
10
21.3
0.2
0.4
1.1
2.:
jects in greater Boston. Water leads
age, sex, education, and dust)
ranged fro* <13 to 208 |ig/d1. Blood
leads ranged from 6 to 71.
PBB = 14.33 ~ 2.541 (PBW)1/3
Worth et al. (1981) study restricted
U.S. EM (1980)
0.023
2
14.3
4.4
5.4
7.4
9.4
to 390 subjects aged 20 or older.
EPA In (PBB) = In (18.6 ~ 0.071 PBW)
0.028
2
18.6
0.4
0.7
1.8
3.6
EM
In (PBB) = In (0.073 PBW ~ other terns
0.153
7
18.8
0.4
0.7
1.8
3.7
for sex, education, and dust)
Worth et al.,(1881) study restricted
U.S. EPA (1980)
PBB = 13.38 ~ 2.487 (PflW)1/3 -
0.030
2
13.4
4.3
5.4
7.3
9.2
to 249 ftaales ages 20 to 50.
EPA
In (PBB) = In (17.6 ~ 0.067 PBW)
0.032
2
17.6
0.3
0.7
1.7
3.4
EPA
In (PfiB) » (0.067 PBW ~ other terms
0.091
6
17.6
0.3
0.7
1.7
3.4
for education and dust)
U.K. Central Directorate (1982)
U.K. Central
PBB = 12.6 * 1.8 (PBW)1/3
0.12
2
12.8
3.1
3.9
5.3
6.6
study of 128 Bothers in greater
Directorate on
Glasgow. Water leads ranged fro*
Environmental
PBB » 18.1 ~ .014 PBW
0.06
2
18.1
0.1
0.1
0.4
0.7
under SO yg/1 (SIX) to over SCO
Pollution
|ig/dl (5X). Blood leads ranged
(1982)
fro* under 5 (jg/d) (ZX) to over
3S pg/dl (5X).
PBB = 7.6 ~ 2.3 (P8W)1/3
U.K. Central Directorate (1982)
U.K. Central
0.22
2
7.6
3.9
5.0
6.7
8.5
study of 126 infants 1n greater
Directorate on
Glasgow. Water leads ranged froa
Environmental
PBB = 16.7 ~ 0.033 PBW
0.12
2
16.7
0.2
0.3
0.8
1.6
under 50 yg/l (61X) to over SOO
Pollution
pg/dl (5X). Blood leads ranged
(1982)
fro* under 5 pg/dl (4X) to over
40 |>g/dl (4X).
Moore (1977) study of 75 residents
Moore (1977)
PBB « 16.6 ~ 0.02 PBW
0.27
2
16.6
0.1
0.2
0.5
1.0
of a Glasgow tenement.
PBB » 4.7 ~ 2.78 (PBW)1/3
Sherlock et al. (1982) study of 114
Sherlock et al.
0.56
2
4.7
4.8
6.0
8.1
10.2
adult women, Blood leads ranged
<5 to >61 pg/dl. Kettle water leads
ranged from <10 to >2570 ua/1.
(1982)
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PRELIMINARY DRAFT
The problem of determining the most appropriate model(s) is essentially equivalent to the
low dose extrapolation problem, since most data sets estimate a relationship that is primarily
based on water lead values from 50 to 2000 pg/dl. The only study that determines the re-
lationship based on lower water lead values (<160,4*8/1) is the Pocock et al, (1983) study.
The data from this study, as well as the authors themselves, suggest that in this lower range
of water lead levels, the relationship is linear. Furthermore, the estimated contributions to
blood lead levels from this study are quite consistent with the polynomial models from other
studies, such as the Worth et al. (1981) and Thomas et al. (1979) studies. For these reasons,
the Pocock et al. (1983) slope of 0.06 is thought to represent the current best estimate. The
possibility still exists, however, that the higher estimates of the other studies may be cor-
rect in certain situations, especially at higher water lead levels (>100 pg/l)-
11.4.3 Studies Relating Lead in Soil and Oust to Blood Lead
The relationship of exposure to lead contained in soil and house dust, and the amount of
lead absorbed by humans, particularly children, has been the subject of scientific investi-
gation for some time (Ouggan and Williams, 1977; Barltrop, 1975; Creason et al., 1975; Barl-
trop et al., 1974; Roberts et al., 1974; Sayre et al., 1974; Ter Haar and Aronow, 1974; Fairey
and Gray, 1970). Ouggan and Williams (1977) published an assessment of the risk of increased
blood lead resulting from the ingestion of lead in dust. Some of these studies have bean con-
cerned with the effects of such exposures (Barltrop, 1975; Creason et al., 1975; Barltrop et
al., 1974; Roberts et al., 1974; Fairey and Gray, 1970); others have concentrated on the means
by which the lead in soil and dust becomes available to the body (Sayre et al., 1974; Ter Haar
and Aronow, 1974).
11.4.3.1 Omaha Nebraska Studies. The Omaha studies were described in Section 11.4.1.7. Soil
samples were 2-inch cores halfway between the building and the lot line. Household dust was
collected from vacuum cleaner bags. The following analysis was provided courtesy of Or.
Angle. The model is also described in Section 11.4.1.8, and provided the following coeffi-
cients and standard errors:
Factor
Coefficient
Asymptotic
Standard Error
Intercept (pg/dl)
Air lead (pg/ma)
Soil lead
-------
PRELIMINARY DRAFT
11.4.3.2 The Stark Study. EPA analyses of data from children in New Haven (Stark et a"!.,
1982) found substantial evidence for dust and soil lead contributions to blood lead, as well
as evidence for increased blood lead due to decreased household cleanliness. These factors
are somewhat correlated with each other; but the separate roles of increased concentration and
clcould be distinguished. The fitted models were summarized earlier (Section
11,3.6.1).
11.4.3.3 The Silver Valley/Kellogg Idaho Study. The Silver Valley Kellogg Idaho study was
discussed in section 11.4.1.6. Yankel et al. (1977) showed .that lead in both soil and dust
was independently related to bltfod lead levels'. In their opinion, 1000 pg/g soil lead ex-
posure was cause for concern. Walter et al. (1980) showed that children aged 3 through 6
showed the strongest relationship between soil lead and blood lead, but 2-year olds and 7-year
olds also had a significant relationship (Table 11-24). The slope of 1.1 for soil lead (1000
pg/g) to blood lead (pg/dl) represents an average relationship for all ages.
The Silver Valley-Kellogg Idaho study also gave some information on house dust lead, al-
though this data was less complete than the other information. Regression coefficients for
these data are in Tables 11-24 and 11-25. In spite of the correlation of these predictors,
significant regression coefficients could be estimated separately for these effects.
11.4.3.4 Charleston Studies. In one of the earliest investigations, Fairey and Gray (1970)
conducted a retrospective study of lead poisoning cases in Charleston, South Carolina. Two-
inch core soil samples were collected from 170 randomly selected sites in the city and were
compared with soil samples taken from homes where 37 cases of lead poisoning had occurred.
.The soil lead values obtained ranged from 1 to 12,000 pg/g, with 75 percent of the samples
containing less than 500 pg/g. A significant relationship between soil lead levels and lead
poisoning cases was established; 500 pg/g was used as the cutpoint in the chi-square contin-
gency analysis. Fairey and Gray were the first to examine this complex problem and, although
their data support the soil lead hypothesis, the relationship between soil lead and blood lead
levels could not be quantified. Furthermore, because no other source of lead was measured,
any positive association could have been confounded by additional sources of lead, such as
paint or air.
A later study by Galke et al. (1975), in Charleston, used a house-to-house survey to re-
cruit 194 black preschool children. Soil, paint and air lead exposures as measured by traffic
density were established for each child. When the population was divided into two groups
based on the median soil lead value (585 pg/g), a 5 pg/dl difference in blood lead levels was
obtained. Soil lead exposure for this population ranged from 9 to 7890 pg/g. Vehicle traffic
patterns were defined by area of recruitment as being high or low. A multiple regression
analysis of the data showed that vehicle traffic patterns, lead level in exterior siding
PB11B/A
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paint, and lead in soil were all independently and significantly related to blood lead levels.
Using the model described in Appendix 11B, the following coefficients and standard errors were
obtained:
Multiple R2 = 0.386
Residual standard deviation = 0.2148 (geometric standard deviation = 1.24)
11.4.3.5 Barltrop Studies. Barltrop et al. (1974) described two studies in England investi-
gating the soil lead to blood lead relationship. In the first study, children aged 2 and 3
and their mothers from two towns chosen for their soil lead content had their blood lead
levels determined from a capillary sample. Hair samples were also collected and analyzed for
lead. Lead content of the suspended particulate matter and soil was measured. Soil samples
for each home were a composite of several 2-inch core samples taken from the yard of each
home. Chemical analysis of the lead content of soil in the two towns showed a 2- to 3-fold
difference, with the values in the control town about 200 to 300 pg/g compared with about 700
to 1000 ug/g In the exposed town. A,difference was also noted in the mean air lead content of
the two towns, 0.60 pg/m3 compared with 0.29 pg/ma. Although this difference existed, both
air lead values were thought low enough not to affect the blood level values differentially.
Mean surface soil lead concentrations for the two communities were statistically different,
the means for the high and low community being 909 and 398 pg/g, respectively. Despite this
difference, no statistically significant differences In maternal blood lead levels or chil-
dren's blood or hair lead levels were noted. Further statistical analysis of the data, using
correlational analysis on either raw or log-transformed blood lead data, likewise failed to
show a statistical relationship of soil lead with either blood lead or hair lead.
The second study was reported in both preliminary and final form (Barltrop et al., 1974;
Barltrop, 1975). In the more detailed report (Barltrop, 1975), children's homes were clas-
sified by their soil lead content into three groups, namely: less than 1,000; 1,000 to
10,000; and greater than 10,000 pg/g. As shown in Table 11-45, children's mean blood lead
levels Increased correspondingly from 20.7 to 29,0 yg/dl. Mean soil lead levels for the low
and high soil exposure groups were 420 and 13,969 pg/g, respectively. Mothers' blood levels,
Factor
Asymptotic
Coefficient Standard Error
Intercept (pg/dl)
Pica (1 = eater, 0 = otherwise)
Traffic Pattern (1 = high, 0 = low)
Siding paint (mg/cm2)
Door paint (mg/cm2)
Soil lead (mg/g)
25.92
7.23
7.11
0.33
0.18
1.46
1.61
1.60
1.48
0.11
0.12
0.59
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however, did not reflect this trend; nor were the children's fecal lead levels different
across the soil exposure areas.
An analysis of the data in Table 11-45 gives the following model;
blood lead (pg/dl) = 0.64 soil lead (1000 pg/g) + 20.98
No confidence intervals were calculated since the calculations were based on means.
TABLE 11-45. MEAN BLOOD AND SOIL LEAD
CONCENTRATIONS IN ENGLISH STUDY
Category
Children's
of soil lead,
Sample
blood lead,
Soil lead,
M9/9
size
Mfl/dl
M9/g
<1000
29
20.7
420
1000-10000
43
23.8
3390
>10000
10
29.0
13969
Source: Barltrop, 1975.
11.4.3.6 The British Columbia Studies. Neri et al. (1978) studied blood lead levels in chil-
dren living in Trail, British Columbia. These blood lead measurements were made by the
capillary method. An episode of poisoning of horses earlier had been traced to ingestion of
lead. Environmental monitoring at that time did not suggest that a human health risk existed.
However, it was later thought wise to conduct a study of lead absorption in the area.
Trail had been the site of a smelter since the turn of the century. The smelter had
undergone numerous changes for reasons of both health and productivity. At the time of the
blood lead study, the smelter was emitting 300 pounds of lead daily, with ambient air lead
3
levels at aboyt 2 Mg/m in 1975. Nelson, BC was chosen as the control city. The cities are
reasonably close (~30 miles distant), are similar in population, and served by the same water
3
basin. The average air lead level in Nelson during the study was 0.5 pg/m .
Initial planning called for the sampling of 200 children in each of three age groups (1-3
years, 1st grade and 9th grade) from each of the two sites. A strike at the smelter at the
onset of the study caused parts of the Trail population to move. Hence, the recruited sample
deviated from the planned one. School children were sampled in May 1975 at their schools
while the 1- to 3-year olds were sampled in September 1975 at a clinic or home. This delayed
sampling was intentional to allow those children to be exposed to the soil and dust for the
entire summer. Blood and hair samples were collected from each child.
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Blood samples were analyzed for lead by anodic stripping voltammetry. The children in
the younger age groups living in Trail had higher blood lead levels than those living in
Nelson. An examination of the frequency distributions of the blood lead levels showed that
the entire frequency of the distribution shifted between the residents of the two cities.
Interestingly, there was no difference in the ninth grade children.
Table 11-46 displays the results of the soil lead levels along with the blood lead levels
obtained in the earlier study. Blood lead levels were higher for 1- to 3-year olds and first
graders in the two nearest-to-smelter categories than in the far-from-smelter category.
Again, no difference was noted for the ninth graders.
An EPA analysis of the Neri et al. (1978) data gives the following models for children 1-
to 3-years old:
Blood lead (pg/dl) = 0.0076 soil lead (pg/g) + 15.43, and
Blood lead (pg/dl) = 0.0046 soil lead (pg/g) + 16.37
for children in grade one. No confidence intervals were calculated since the analysis was
based on means.
TABLE 11-46. LEAD CONCENTRATION OF SURFACE SOIL AND CHILDREN'S
BLOOD BY RESIDENTIAL AREA OF TRAIL, BRITISH COLUMBIA
Residential
area(s)
Mean
soil lead
concentration (pg/g)
± standard error
(and no. of samples)
Blood lead concentration
(pg/dl), mean ± standard
error (and no. of children)
1- to 3-
year olds
Grade one
children
1 and 2
5
9
3, 4, and 8
6 and 7
225
777
570
1674
1800
39
239
143
183
(26)
(12)
(11)
(53)
± 212 (51)
17.2
19.7
20.7
27.7
30.2
1.1
1.5
(27)
(11)
± 1.6 (19)
±1.8 (14)
+ 3.0 (16)
18.0 ±
18.7 ±
19.7 ±
23.8 t
25.6 ±
1.9
2.3
(18)
(12)
1.0 (16)
1.3 (31)
1.5 (26)
Total
1320 ± 212 (153)
22.4 ± 1.0 (87) 21.9 ± 0.7 (103)
Source: Schmitt et al., 1979.
11.4.3.7 Other Studies of Soil and Dusts. Lepow et al. (1975) studied the lead content of
air, house dust and dirt, as well as the lead content of dirt on hands, food and water, to
determine the cause of chronically elevated blood lead levels in 10 children 2- to 6-years-old
PB11B/A 11-106 7/29/83
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in Hartford, Connecticut. Lead-based paints had been eliminated as a significant source of
lead for these children. Ambient air lead concentrations varied from 1.7 to 7.0 pg/ffl^. The
Bean lead concentration in dirt was 1,200 pg/g and in dust, 11,000 pg/g. The wean concentra-
tion of lead in dirt on children's hands was 2,400 pg/g, The mean weight of samples of dirt
fro* hands was 11 mg, which represented only a small fraction of the total dirt on hands. Ob-
servation of the mouthing behavior in these young children led to the conclusion that the
hands-in-mouth exposure route was the principal cause of excessive lead accumulation.
Several studies have investigated the mechanism by which lead from soil and dust gets in-
to the body (Sayre et al., 1974; Ter Haar and Aronow, 1974). Sayre et al. (1974) in
Rochester, New York, demonstrated the feasibility of house dust as a source of lead for chil-
dren. Two groups of houses, one inner city and the other suburban, were chosen for the study.
Lead-free sanitary paper towels were used to collect dust samples front house surfaces and the
hands of children (Vostal et al., 1974). The medians for the hand and household samples were
used as the cutpoints in the chi-square contingency analysis. A statistically significant
difference between the urban and suburban homes for dust levels was noted, as was a relation-
ship between household dust levels and hand dust levels (Lepow et al., 1975).
Ter Haar and Aronow (1974) investigated lead absorption in children that can be at-
tributed to ingestion of dust and dirt. They reasoned that because the proportion of the
naturally occurring isotope of 2l0Pb varies for paint chips, airborne particulates, fallout
dust, house dust, yard dirt and street dirt, it would be possible to identify the sources of
ingested lead. They collected 24-hour excreta from eight hospitalized children on the first
day of hospitalization. These children, 1- to 3-years old, were suspected of having elevated
body burdens of lead, and one criterion for the suspicion was a history of pica. Ten children
of the same age level, who lived in good housing in Detroit and the suburbs, were selected as
controls and 24-hour excreta were collected from them. The excreta were dried and stable lead
as well as 2l0Pb content determined. For seven hospitalized children, the stable lead mean
value was 22.43 pg/g dry excreta, and the eighth child had a value of 1640 yq/g. The con-
trols1 mean for stable lead was 4.1 pg/g dry excreta. However, the respective means for 210Pb
expressed as pCi/g dry matter were 0.044 and 0.040. The authors concluded that because there
is no significant difference between these means for 210Pb, the hypothesis that young children
with pica eat dust is not supported. The authors further concluded that children with
evidence of high lead intake did not have dust and air suspended particulate as the sources of
their lead. It is clear that air suspended particulate did not account for the lead levels in
the hospitalized children. However, the 21QPb concentrations in dust and feces were similar
for all children, making it difficult to estimate the dust contribution.
Heyworth et al. (1981) studied a population of children exposed to lead in mine tailings.
These tailings were used in foundations and playgrounds, and had a lead content ranging from
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10,000 to 15,000 |jg/g. In December 1979 venous blood samples and hair were collected from 181
of 346 children attending two schools in Western Australia. One of the schools was a primary
school; the other was a combined primary and secondary school. Parents completed question-
naires covering background information as well as information regarding the children's expo-
sure to the tailings. Blood lead levels were determined by the AAS method of Farrely and
Pybos. Good quality control measures were undertaken for the study, especially for the blood
lead levels. Blood lead levels were higher in boys vs. girls (mean values were 14.0 and 10.4
|jg/dl, respectively). This difference was statistically significant. Five percent of the
children (n = 9} had blood lead levels greater than 25 pg/dl. Five of the children had blood
lead levels greater than 30 pg/dl. Blood lead levels decreased significantly with age and
were slightly lower in children living on properties on which tailings were used. However,
they were higher for children attending the school that used the tailihgs in the playground.
Landrigan et al. (1982) studied the impact on soil and dust lead levels on removal of
leaded paint from the Mystic River Bridge in Masschusetts. Environmental studies in 1977 in-
dicated that surface soil directly beneath the bridge had a lead content ranging from 1300 to
1800 pg/g. Analysis of concomitant trace elements showed that the lead came from the bridge.
A concurrent survey of children living in Chelsea (vicinity of bridge) found that 49 percent
of 109 children had blood lead levels greater than or equal to 30 pg/dl- Of children living
more distant from the bridge "only" 37 percent had that level of blood lead.
These findings prompted the Massachusetts Port Authority to undertake a program to delead
the bridge. Paint on parts of the bridge that extended over neighborhoods was removed by
abrasive blasting and replaced by zinc primer. Some care was undertaken to minimize both the
occupational as well as environmental exposures to lead as a result of the blasting process.
Concurrently with the actual deleading work, a program of air monitoring was established
to check on the environmental lead exposures being created. In June 1980 four air samples
3
taken at a point 27 meters from the bridge had a mean lead content of 5.32 pg/m . As a result
of these findings air pollution controls were tightened; mean air lead concentrations 12
3
meters from the bridge in July were 1.43 pg/m .
Samples of the top 1 cm of soil were obtained in July 1980 from within 30, 30 to 80, and
100 meters from the bridge. Comparison samples from outside the area were also obtained.
Samples taken directly under the bridge had a mean lead content of 8127 pg/g.
Within 30 meters of the bridge, the mean content was 3272 pg/g, dropping to 457 pg/g at 30 to
80 meters. At 100 meters the soil lead level dropped to 197 pg/g. Comparison samples ranged
from 83 to 165 pg/g depending on location.
Fingerstick blood samples were obtained on 123 children 1-5 years of age living within
0.3 km of the bridge in Charlestown. Four children (3.3 percent) had blood lead levels
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greater than 30 with a maximum of 35 (ig/dT- All four children lived within two blocks
of the bridge. Two of the four had lead paint in their homes but it was intact. None of the
76 children living more than two blocks from the bridge had blood leads greater than or equal
to 30 pg/dl, a statistically significant difference.
She!Shear's (1973) case report from New Zealand ascribes a medically diagnosed case of
lead poisoning to high soil lead content in the child's home environment. Shellshear et al.
(1975) followed up his case report of increased lead absorption resulting from exposure to
lead contaminated soil with a study carried out in Christchurch, New Zealand. Two related
activities comprised the study. First, from May 1973 to November 1973, a random study of
pediatric admissions to a local hospital was made. Blood samples were taken and analyzed for
lead. Homes were visited and soil samples were collected and analyzed for lead, lead anal-
yses for both soil and blood were conducted by MS. Second, a soil survey of the area was
undertaken. Whenever a soil lead value greater than 300 yg/g was found and a child aged one
to five was present, the child was referred for blood testing.
The two methods of subject recruitment yielded a total of 170 subjects. Eight (4.7 per-
cent) of the children had blood lead equal to or greater than 40 pg/dl, and three of them had
a blood lead equal to or greater than 80 pg/dl. No correlation with age was noted. The mean
blood lead of the pediatric admissions was 17.5 pg/dl with an extremely large range (4 to 170
pg/dl). The mean blood lead for soil survey children was 19.5 pg/dl.
Christchurch was divided into two sections based on the date of development of the area.
The inner area had developed earlier and a higher level of lead was used there in the house
paints. The frequency distribution of soil lead levels showed that the inner zone samples had
much higher soil lead levels than the outer zone. Furthermore, analysis of the soil lead
levels by type of exterior surface of the residential unit showed that painted exteriors had
higher soil lead values than brick, stone or concrete block exteriors.
Analysis of the relationship between soil lead and blood lead was restricted to children
from the sampled hospital who had lived at their current address for at least 1 year. Table
11-47 presents the analysis of these results. Although the results were not statistically
significant, they are suggestive of an association.
Analysis of the possible effect of pica on blood lead levels showed the mean blood lead
for children with pica to be 32 pg/dl while those without pica had a mean of 16.8 jjg/dl. The
pica blood lead mean was statistically significantly higher than the non-pica mean.
Wedeen et al. (1978) reported a case of lead nephropathy in a black female who exhibited
geophagia. The patient, who had undergone chelation therapy, eventually reported that she had
a habit of eating soil from her garden in East Orange, New Jersey. During spring and summer,
she continuously kept soil from her garden in her mouth while gardening. She even put a sup-
ply away for winter. The soil was analyzed for lead and was found to contain almost 700 pg/g.
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TABLE 11-47. ANALYSIS Of RELATIONSHIP BETWEEN SOIL LEAD AND BLOOD
LEAD IN CHILDREN
Soil
lead (uq/q)
Blood lead ug/dl)
Area of city
Mean
Range n
Mean
Range
Inner zone
1950
30-11000 21
25.4
4-170
Outer zone
150
30-1100 47
18.3
5-84
Source: Shell shear (1973).
The authors estimated that the patient consumed 100 to 500 mg of lead each year. One month
after initial hospitalization her blood lead level was 70 pg/dl.
11.4.3.8 Summary of Soil and Dust Lead . Studies relating soil lead to blood lead levels are
difficult to compare. The relationship obviously depends on depth of soil lead, age of the
children, sampling method, cleanliness of the home, mouthing activities of the children, and
possibly many other factors. Table 11-48 gives some estimated slopes taken from several dif-
ferent studies. The range of these values is quite large, ranging from 0.6 to 7.6. The
values from the Stark et al. (1980) study of about 2 pg/dl per mg/g represent a reasonable
median estimate.
The relationship of house dust lead to blood lead is even more difficult to obtain.
Table 11-49 contains some values for three studies that give data permitting such caculations.
The median value of 1.8 pg/dl per mg/g for 2-3 years old in the Stark study may also represent
a reasonable value for use here.
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TABLE 11-48. ESTIMATES OF THE CONTRIBUTION OF SOIL LEAD
TO BLOOD LEAD
Study
Range of soil
lead values
(M/g)
Depth of
sample
Estimated ,
slope (X10 )
Sample
size
R2
Angle and Mclntire
(198?) study of
children in
Omaha, NE
16 to 4792
2"
6,8
1075
.198
Stark et al.
(1982) study
of children
New Haven, CT
30 to 7000
(age 0-1)
30 to 7600
(age 2-3)
V
2.2
2.0
153
334
.289
.300
Yankel et al.
(1977) study
of children
in Kellogg, ID
50 to 24,600
3/4"
1.1
860
.662
6a!ke et al.
(1975)
study of
chilren in
Charleston, SC
9 to 7890
2"
1.5
194
.386
Barltrop et
al. (1975)
study of
children in
England
420 to 13,969
(group means)
2"
0.6
82
NA*
Neri et al.
(1978) study
of children
in British
Columbia
225-1800
(group means,
age 1-3)
225-1800
(group means,
age 2-3)
NA
NA
7.6
4.6
87
103
NA
NA
*NA means Not Available.
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TABLE 11-49. ESTIMATES OF THE CONTRIBUTION OF
HQUSEDUST TO BLOOD LEAD IN CHILDREN
Study
Range of dust
Lead values (pg/g)
Age range
in years
Estimated ,
slope (X10 )
Sample
Size
»2
R
Angle and Mclntire
(1979) study in
Omaha, NE
18-5571
1-18
6-18
7.18
3.36
1074
832
.198
.262
Stark et al. (1982)
study in New Haven,
CT
70-7600
40-7600
9-4900
0-1
2-3
4-7
4.02
1.82
0.02
153
334
439
.289
.300
.143
Yankel et al. (1977)
study in Kellogg,
ID
50-35,600
0-4
5-9
0.19
0.20
185
246
.721
.623
11.4.4 Paint Lead Exposures
A major source of environmental lead exposure for the general population comes from lead
contained in both interior and exterior paint on dwellings. The amount of lead present, as
well as its accessibility, depends upon the age of the residence (because older buildings
contain paint manufactured before lead content was regulated) and the physical condition of
the paint. It is generally accepted by the public and by health professionals that lead-based
paint is one major source of overtly symptomatic pediatric lead poisoning in the United States
(Lin-Fu, 1973).
The level and distribution of lead paint in a dwelling is a complex function of history,
geography, economics, and the decorating habits of its residents., Lead pigments were the
first pigments produced on a large commercial scale when the paint Industry began its growth
in the early 1900's. In the 1930's lead pigments were gradually replaced with zinc and other
opacifiers. By the 1940's, titanium dioxide became available and is now the most commonly
used pigment for residential coatings. There was no regulation of the use of lead in house
paints until 1955, when the paint industry adopted a voluntary standard that limited the lead
content in interior paint to no more than 1 percent by weight of the nonvolatile solids. At
about the same time, local jurisdictions began adopting codes and regulations that prohibited
the sale and use of interior paints containing more than 1 percent lead (Berger, 1973a,b).
In spite of the change in paint technology and local regulations governing its use, and
contrary to popular belief, interior paint with significant amounts of lead was still availa-
ble in the 1970's. Studies by the National Bureau of Standards (1973) and by the U.S.
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Consumer Product Safety Commission (1974) showed a continuing decrease in the number of in-
terior paints with lead levels greater than 1 percent. By 1974, only 2 percent of the in-
terior paints sampled were found to have greater than 1 percent lead in the dried film (U.S.
Consumer Product Safety Commission, 1974).
The level of lead in paint in a residence that should be considered hazardous remains in
question. Not only is the total amount of lead in paint important, but also the accessibility
of the painted surface to a child, as well as the frequency of ingestion must be considered.
Attempts to set an acceptable lead level, in situ, have been unsuccessful, and preventive con-
trol measures of lead paint hazards has been concerned with lead levels in currently manu-
factured paint. In one of its reviews, the NAS concluded: "Since control of the lead paint
hazard is difficult to accomplish once multiple layers have been applied in homes over two to
three decades, and since control is more easily regulated at the time of manufacture, we re-
commend that the lead content of paints be set and enforced at time of manufacture" (National
Academy of Sciences, 1976).
Legal control of lead paint hazards is being attempted by local communities through
health or housing codes and regulations. At the Federal level, the Department of Housing and
Urban Development has issued regulations for lead hazard abatement in housing units assisted
or supported by its programs. Generally, the lead level considered hazardous ranges from 0.5
2
to 2.5 mg/cm , but the level of lead content selected appears to depend more on the sensiti-
vity of field measurement (using X-ray fluorescent lead detectors) than on direct biological
dose-response relationships. Regulations also require lead hazard abatement when the paint is
loose, flaking, peeling or broken, or in some cases when it is on surfaces within reach of a
child's mouth.
Some studies have been carried out to determine the distribution of lead levels in paint
in residences. A survey of lead levels in 2370 randomly selected dwellings in Pittsburgh pro-
vides some indication of the lead levels to be found (Shier and Hall, 1977). Figure 11-22
shows the distribution curves for the highest lead level found in dwellings for three age
groupings. The curves bear out the statement often made that paint with high levels of lead
is most frequently found in pre-1940 residences. One cannot assume, however, that high lead
paint is absent in dwellings built after 1940. In the case of the houses surveyed in
Pittsburgh, about 20 percent of the residences built after 1960 have at least one surface with
more than 1.5 mg/cm .
The distribution of lead within an individual dwelling varies considerably. Lead paint
is most frequently found on doors and windows where lead levels greater than 1.5 mg/cm2 were
found on 2 percent of the surfaces surveyed, whereas only about 1 percent of the walls had
2
lead levels greater than 1.5 mg/cm (Shier and Hall, 1977).
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0.8
0.7
PRE 1940: N = 2525
0.6
OS
1940 1960; N = 178
04
0.3
0.2
I960 1975: N = 27
0.1
0
3
1
2
4
5
LEAD LEVEL (X», mfj/cm2
Figure 11-22. Cumulative distribution of lead levels in dwelling units.
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In a review of the literature (Lin-Fu, 1973) found general acceptance that the presence
of lead in paint is necessary but not sufficient evidence of a hazard. Accessibility in
terms of peeling, flaking or loose paint also provide evidence for the presence of a hazard.
Of the total samples surveyed, about 14 percent of the residences had accessible paint with a
2
lead content greater than 1.5 mg/cm, As discussed in Section 7.3.2.1.2, one must note that
lead oxides of painted surfaces contribute to the lead level of house dust.
It is not possible to extrapolate the results of the Pittsburgh survey nationally; how-
ever, additional data from a pilot study of 115 residences in Washington, DC, showed similar
results (Hall 1974).
An attempt was made in the Pittsburgh study to obtain information about the correlation
between the quantity and condition of lead paint in buildings, and the blood lead of children
who resided there (Urban, 1976). Blood lead analyses and socioeconomic data for-456 children
were obtained, along with the information about lead levels in the dwelling. Figure 11-23 is
a plot of the blood lead levels vs. the fraction of surfaces within a dwelling with lead
2
levels of at least 2 mg/cm . Analysis of the data shows a low correlation between the blood
lead levels of the children and fraction of surfaces with lead levels above 2 mg/cm , but
there is a stronger correlation between the blood lead levels and the condition of the painted
surfaces in the dwellings in which children reside. This latter correlation appeared to be
independent of the lead levels in the dwellings.
Two other studies have attempted to relate blood lead levels and paint lead as determined
by X-ray fluorescence. Reece et al. (1972) studied 81 children from two lower socioeconomic
communities in Cincinnati. Blood leads were analyzed by the dithizone method. There was con-
siderable lead in the home environment, but it was not reflected in the children's blood lead.
Analytical procedures used to test the hypothesis were not described; neither were the raw
data presented.
Galke et al. (1975), in their study of inner city black children measured the paint lead,
both interior and exterior, as well as soil and traffic exposure. In a multiple regression
analysis, exterior siding paint lead was found to be significantly related to blood lead
levels.
Evidence indicates that a source of exposure in childhood lead poisoning is peeling lead
paint and broken lead-impregnated plaster found in poorly maintained houses. There are also
reports of exposure cases that cannot be equated with the presence of lead paint. Further,
the analysis of paint in homes of children with lead poisoning has not consistently revealed a
hazardous lead content (Lin-Fu, 1973). For example, one paper reported 5466 samples of paint
obtained from the home environment of lead poisoning cases in Philadelphia between 1964 and
1968. Among these samples of paint, 67 percent yielded positive findings, i.e., paint with
more than 1 percent lead (Tyler, 1970).
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!
V)
•" iu
2 >
£ 5
fiC
9 Q
5 <
X ui
u -I
o
o
o
-J
CD
30
25
20
15
~iiiiiir
SURFACES IN BAD CONDITION, i.e., PEELING,
CHALKING, OR POOR SUBSTRATE
ALL SURFACES
«o
mfym
»1
1
I
1
0.1 0.2 0.3 0.4 0.5 0.6 0.7
FRACTIONS OF SURFACES WITH LEAD >2 mg/cm
0.8 0.9
2
1.0
Figure 11-23. Correlation of children's blood lead levels with fractions of surfaces
within a dwelling having lead concentrations > 2 mg Pb/cm*.
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Data published or made available by the Centers for Disease Control also show that a sig-
nificant number of children with undue lead absorption occupy buildings that were inspected
for lead-based paint hazards, but in which no hazard could be demonstrated (U.S. Centers for
Disease Control, 1977a; Hopkins and Houk, 1976). Table 11-50 summarizes the data obtained
frc:,-, the HEW funded lead-based paint poisoning control projects for Fiscal Years 1981, 1979,
1978, 1975, and 1974. These data show that in Fiscal Years 1974, 1975, and 1978, about 40 to
50 percent of confirmed cases of elevated blood lead levels, a possible source of lead paint
hazard could not be located. In fiscal year 1981, the U.S. Centers for Disease Control
(1982a,b), screened 535,730 children and found 21,897 with lead toxicity. Of these, 15,472
dwellings were inspected and 10,666 or approximately 67 percent were found to have leaded
paint. The implications of these findings are not clear. The findings are presented in order
to place in proper perspective both the concept of total lead exposure and the concept that
lead paint is one source of lead that contributes to the total body load. The background con-
tribution of lead from other sources is still not known, even for those children for whom a
potential lead paint hazard has been identified; nor is it known what proportion of lead came
from which source.
TABLE 11-50. RESULTS OF SCREENING AND HOUSING INSPECTION IN CHILDHOOD LEAD
POISONING CONTROL PROJECT 8Y FISCAL YEAR
Fiscal Year
Results
1981
1979
1978
1975
1974
Children screened
535,730
464,751
397,963
440,650
371,955
Children with elevated
lead exposure
21,897
32,537
25,801
28,597a
16,228a
Dwellings inspected
15,472
17,911
36,138
30,227
23,096
Dwellings with
lead hazard
10,666
12,461
18,536
17,609
13,742
Confirmed blood lead level >40 pg/dl.
Source: U.S. Centers for Disease Control (1977a, 1979, 1980, 1982a,b);
Hopkins and Houk, 1976.
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11.5 SPECIFIC SOURCE STUDIES
The studies reviewed in this section all provide important information regarding specific
environmental sources of airborne lead that play* significant role in population blood lead
levels. These studies also illustrate several interesting approaches to this issue.
11.5.1 Combustion of Gasoline Antiknock Compounds
11.5.1,1 Isotope Studies, Two field investigations have attempted to derive estimates of
the amount of lead from gasoline that is absorbed by the blood of individuals. Both of these
investigations used the fact that non-radioactive isotopes of lead are stable. The varying
proportions of the isotopes present in blood and environmental samples can indicate the source
of the lead. The Isotopic Lead Experiment (ILE) 1s an extensive study that attempted to use
differing proportions of the isotopes in geologic formations to infer the proportion of lead
in gasoline that is absorbed by the body. The other study utilized existing natural shifts in
isotopic proportions in an attempt to do the same thing.
11,5.1.1.1 Italy. The ILE is a large scale community study in which the geologic source of
lead for antiknock compounds in gasoline was manipulated to change the isotopic composition of
the atmosphere (Garibaldi et al., 1975; Facchetti, 1979). Preliminary investigation of the
environment of Northwest Italy, and the blood of residents there, indicated that the ratio of
lead 206/207 in blood was a constant, about 1.16, and the ratio in gasoline was about 1.18.
This preliminary study also suggested that it would be possible to substitute for the curren-
tly used geologic sources of lead for antiknock production, a geologically distinct source of
lead from Australia that had an isotopic 206/207 ratio of 1.04. It was hypothesized that the
resulting change in blood lead 206/207 ratios (from 1.16 to a lower value) would indicate the
proportion of lead in the blood of exposed human populations attributable to lead in the air
contributed by gasoline combustion in the study area.
Baseline sampling of both the environment and residents in the geographic area of the
study was conducted in 1974-75. The sampling included air, soil, plants, lead stock, gasoline
supplies, etc. Human blood sampling was done on a variety of populations within the area.
Both environmental and human samples were analyzed for lead concentrations as well as isotopic
206/207 composition.
In August 1975 the first switched (Australian lead labelled) gasoline was introduced;
although it was originally intended to get a 100 percent substitution, practical and logisti-
cal problems resulted in only a 50 percent substitution being achieved by this time. By May
1977, these problems were worked out and the substitution was practically complete. The sub-
stitution was maintained until the end of 1979, when a partial return to use of the original
sources of lead began. Therefore, the project had. four phases; phase zero - background;
phase one - partial switch; phase two - total switch; and phase three - switchback.
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Airborne lead measurements were collected In a number of sites to generate estimates of
the lead exposure that was experienced by residents of the area. Turin, the major city of the
region, was found to have a much "greater- level of atmospheric lead than the surrounding
countryside. There also appeared to be fairly wide seasonal fluctuations.
The isotopic lead ratios obtained in the samples analyzed are displayed in Figure 11-24.
It can easily be seen that the airborne particulate lead rapidly changed its isotope ratio in
line with expectations. Changes in the isotope ratios of the blood samples appeared to lag
somewhat behind. Background blood lead ratios for adults were 1.1591 ± 0.0043 in rural areas
and 1.1627 i 0.0022 in Turin in 1975. For Turin adults, a mean isotopic ratio of 1.1325 was
obtained in 1979, clearly less than background. Isotopic ratios for Turin schoolchildren,
obtained starting in 1977, tended to be somewhat lower than the ratios for Turin adults.
Preliminary analysis of the isotope ratios in air lead allowed for the estimation of the
fractional contribution of gasoline in the city of Turin, in small communities within 25 km of
Turin, and in small communities beyond 25 km (Facchetti and Geiss, 1982). At the time of
maximal use of Australian lead isotope in gasoline (1978-79), about 87,3 percent of the air
lead in Turin and 58.7 percent of the air lead in the countryside was attributable to
gasoline. The determination of lead isotope ratios was essentially independent of air lead
concentrations. During that time, air lead averaged about 2.0 ms/® in Turin (from 0.88 to
3 3
4.54 pg/m depending on location of the sampling site), about 0.56 pg/m in the nearby com-
munities (0.30 to 0.67 pg/m3) and about 0.30 pg/m"* in more distant (> 25 km) locations.
Blood lead concentrations and isotope ratios for 35 adult subjects were determined on two
or more occasions during phases 0-2 of the study (see Appendix C). Their blood lead isotope
ratios decreased over time and the fraction of lead in their blood attributable to the
Australian lead-labelled gasoline could be estimated independently of blood lead concentration
(see Appendix C for estimation method). The mean fraction, of blood lead attributable to the
Australian lead-labelled gasoline ranged from 23.7 ±5.4 percent in Turin to 12.5 ± 7.1 per-
cent in the nearby (< 25 km) countryside and 11.0 ± 5.8 percent in the remote countryside.
These likely represent minimal estimates of fractions of blood lead derived from gasoline due
to: (1) use of some non-Australian lead-labelled gasoline brought into the study area from
outside; (2) probable insufficient time to have achieved steady-state blood lead isotope
ratios by the time of the switchback; (3) probable insufficient time to fully reflect delayed
movement of the Australian lead from gasoline via environmental pathways in addition to air.
These results can be combined with the actual blood lead concentrations to estimate the
fraction of gasoline uptake attributable or not attributable to direct inhalation. The
results are shown in Table 11-51 (based on a suggestion by Dr. Facchetti). From Section
11.4.1, we conclude that an assumed value of 0=1.6 is plausible for predicting the amount of
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1.20
1.18
1.18
1.14
1.12
1.10
1.06
1.06
I I I I I I I I I I II I II I I
•} BASED ON A LIMITED NUMBER OF SAMPLES
- Pb 206/Pb 207
BLOOD
* _
>•
ADULTS < 25 km
ADULTS > 26 km
ADULTS TURIN
TRAFFIC WARDENS-TURIN
SCHOOL CHILDREN-TURIN
AIRBORNE
PARTICULATE
• TURIN
A COUNTRYSIDE
O PETROL
PfWM 0
Phase 1
4*-
Phate 2
Phas« 3
1 M I i 1 M I I M I t I I I
74
7S
76
77
78
79
80
81
Figure 11-24. Change in Pb-206/Pb-207 ratios in petrol, airborne particulate,
and blood from 1974 to 1981.
Source; Facchettf and Geiss (1982).
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TABLE 11-51. ESTIMATED CONTRIBUTION OF LEADED GASOLINE TO BLOOO LEAD
BY INHALATION AND NON-INHALATION PATHWAYS
Air Lead
Fraction
From
Blood Pb Blood PB Non- Estimated
Mean Fraction Mean PB From Inhaled Fraction
Air From Blood From Gaso- Pb Fro* Gas-Lead
(ng/dl) (pg/dl) (ng/dl) (pg/dl)
Location
Turin 0.873 2.0 0.237 21.77 5.16 2.79 2.37 0.54
<25 km 0.587 0.56 0.125 25.06 3.13 0.53 2.60 0.17
>25 ka 0.587 0.30 0.110 31.78 3.50 0.28 3.22 0.08
(a) Fraction of air lead in Phase 2 attributable to lead in gasoline.
(b) Mean air lead in Phase 2, Mg/m3.
(c) Mean fraction of blood lead in Phase 2 attributable to lead in gasoline.
(d) Mean blood lead concentration in Phase 2, jig/dl.
(e) Estiaated blood lead from gasoline = (c) x (d)
(f) Estimated blood lead from gas inhalation = p x (a) x (b), 0 * 1.6.
(g) Estimated blood lead fro* gas, non-inhalation = (f)-(e)
(h) Fraction of blood lead uptake from gasoline attributable to direct inhalation = (f)/(e)
Data: Facchetti and Geiss (1982), pp. 52-56.
lead absorbed into blood at air lead concentrations less than 2.0 pg/n'. The predicted values
for lead fro* gasoline in air (in the ILE) range fro« 0.28 to 2.79 |jg/d1 in blood due to
direct inhalation. The total contribution of blood lead fro» gasoline is nuch larger, fro«
3.50 to 5.16 jig/dl, suggesting that the non-inhalation contribution of gasoline increases from
2.37 pg/dl in Turin to 2.60 pg/dl in the near region and 3.22 jjg/dl in the more distant region.
The non-inhalation sources include ingestion of dust and soil lead, and lead in food and
drinking water. Efforts are being made to quantify the magnitude of these sources. The aver-
age direct inhalation of lead in the air from gasoline is 8 to 17 percent of the total
intake attributable to gasoline in the countryside and an estimated 68 percent in the city
of Turin. Note that in this sample, the blood lead concentrations are least in the city and
highest in the nore remote areas. This is not obviously attributable to sex because the city
saaple was all male. A more detailed statistical investigation is needed.
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Lead uptake may also be associated with occupation, sex, age, smoking and drinking
habits. The linear exposure model used in Section 11.4 was also used here to estimate the
fraction of labelled blood lead from gasoline attributable to exposure via direct inhalation
and other pathways. EPA used blood lead measurements in Phase 2 for the 35 subjects for whom
repeated measurements allowed estimation of the change in isotope ratios in the blood. Their
blood lead concentrations in Phase 2 were also determined, allowing for estimation of the total
gasoline contribution to blood lead. Possible covariates included sex, age, cigarette
smoking, drinking alcoholic beverages, occupation, residence location and work location. In
order to obtain some crude comparisons with the inhalation exposure studies of Section 11.4.1,
EPA analysis assigned the air lead values listed in Table 11-52 to various locations. Lower
values for air lead in Turin would increase the estimated blood lead inhalation slope above
the estimated value 1.70. Since the fraction of time subjects were exposed to workplace air
was not known, this was also estimated from the data as about 41 percent (i.e., 9.8 hours/day).
The results are shown in Figure 11*25 and Table 11-53. Of all the available variables, only
location, sex and inhaled air lead from gasoline proved statistically significant in predic-
2
ting blood lead attributable to gasoline. The model predictability is fairly good, R = 0.654.
It should be noted that a certain amount of confounding of variables was unavoidable in this
small set of preliminary data, e.g., no female subjects in Turin or in occupations of traffic
wardens, etc. There was a systematic increase in estimated non-inhalation contribution from
gasoline increase for remote areas, but the cause is unknown. Nevertheless, the estimated
non-inhalation contribution of gasoline to blood lead in the ILE study is significant (i.e.
1.8 to 3.4 Mg/dl).
TABLE 11-52. ASSUMED AIR LEAD CONCENTRATIONS FOR MODEL
Residence or workplace code 1-4 5 6
Location outside Turin Turin residential Turin central
Air lead concentration (a) 1.0 pg/m3^ 2.S pg/m3^
(a) Use value for community air lead, 0.16 to 0.67 pg/m .
3 3
(b) Intermediate between average traffic areas (1.71 g/m ) and low traffic areas (0.88 g/m )
in Turin.
(c) Intermediate between average traffic areas (1.71 pg/m ) and heavy traffic areas (4.54
g/m ) in Turin.
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The preliminary linear analysis of the overall ILE data set (2161 observations) found
that total blood lead levels depended on other covariates for which there were plausible
mechanisms of lead exposure, including location, smoking, alcoholic beverages, age and occu-
pation (Facchetti and Geiss 1982). The difference between total blood lead uptake and blood
Total contribution of
gasoline load to
blood lead In — , -
Italian men.
Noninhalation contribution
of gasotine to blood load
In Italian man.
Contribution to blood laad
by direct inhalation from
air laad attributable to
gaeollne.
AVERAGE AIR LEAD CONCENTRATION ATTRIBUTABLE TO QA80UNE
Mfl/m*
Figure 11-25. Estimated direct and indirect contributions of lead in
gasoline to blood lead in Italian men, based on EPA analysis of
ILE data (Table 11-63).
lead uptake attributable to gasoline lead has yet to be analyzed in detail, but these analyses
suggest that certain important differences may be found. Some reservations have been expres-
sed about the ILE study, both by the authojs themselves and by Elwood (1983). These include
unusual conditions of meteorology and traffic in Turin, and demographic characteristics of the
35 subjects measured repeatedly that may restrict the generalizability of the study. However,
it is clear that changes in air lead attributable to gasoline were tracked by changes in blood
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TABLE 11-53. REGRESSION MODEL FOR BLOOD LEAD ATTRIBUTABLE TO GASOLINE
Variable
Coefficient t Standard Error
Air lead from gas
1.70 ± 1.04 (jg/dl per pg/m
LOCATION
Turin
<25 km
>25 km
1.82 ± 2.01 pg/dl
2.56 ± 0.59 pg/dl
3.42 ± 0.85 pg/dl
Sex
-2,03 ± 0.48 pg/dl for women
lead in Turin residents. The airborne particulate lead isotope ratio quickly achieved new
equilibrium levels as the gasoline isotope ratio was changed, and maintained that level during
the 2\ years of Phase 2. The blood lead isotope ratios fell slowly during the changeover
period, and rose again afterwards as shown in Figure 11-24. Equilibrium was not clearly
achieved for blood lead isotope ratios, possibly due to large endogenous pools of old lead
stored in the skeleton and slowly mobilized over time. Even with such reservations, this
study provides a useful basis for relating blood lead and air lead derived from gasoline com-
bustion.
11.5.1.1.2 United States. Manton (1977) conducted a long term study of 10 subjects whose
blood lead isotopic composition was monitored for comparison with the isotopic composition of
the air they breathed. Manton had observed that the ratio of 266Pb/264Pb in the air varied
with seasons in Dallas, Texas; therefore, the ratio of those isotopes should vary in the
blood. By comparing the observed variability, estimates could then be made of the amount of
lead in air that is absorbed by the blood.
Manton took monthly blood samples from all 10 subjects from April 1974 until June 1975.
The blood samples were analyzed for both total lead and isotopic composition. The recruited
volunteers included a mix of males and females, and persons highly and moderately exposed to
lead. However, none of the subjects was thought to be exposed to more than 1 pg/m of lead in
air. Lead in air samples was collected by Hi-Vol samplers primarily from one site in Dallas.
That site, however, had been shown earlier to vary in isotopic composition paralleling another
site some 16 miles away. All analyses were carried out under clean conditions with care and
caution being exercised to avoid lead contamination.
The isotope ratio of lead 206Pb/804Pb increased linearly with time from about 18.45 to
19.35, approximately a 6 percent increase. At least one of the two isotopic lead ratios in-
creased linearly in 4 of the 10 subjects. In one other, they increased but erratically. In
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the remainder of the subjects, the isotopic ratios followed smooth curves showing inflection
points. The curves obtained for the two subjects born in South Africa were 6 months out of
phase with the curves of the native-born Americans. The fact that the isotope ratios in 9 of
the 10 subjects varied regularly was thought to indicate that the non-airborne sources of lead
varied in isotopic composition very slowly.
The blood lead levels exhibited a variety of patterns, although none of the subjects
showed more than a 25 percent change from initial levels. This suggests a reasonably steady
state external environment.
Manton carried his analyses further to estimate the percentage of lead in blood that
comes from air. He estimated that the percentage varied from 7 to 41 percent, assuming that
dietary sources of lead had a constant isotopic ratio while air varied. He calculated the
percent contribution according to the following equation:
—9— = JL > where
100+q a
b = rate of change of an isotope ratio in blood,
a = rate of change of the same ratio in the air,
q = constant - the number of atoms of the isotope in the denominator
of the airborne lead ratio mixed with 100 atoms of the same iso-
tope of lead from non-airborne sources.
The results are shown in Table 11-54. Slopes were obtained by least squares regression.
Percentages of airborne lead in blood varied between 7±3 and 4113.
TABLE 11-54. RATE OF CHANGE OF 2<>6Pb/204Pb AND 20epb/2C7pb
IN AIR AND BL000, AND PERCENTAGE OF AIRBORNE
LEAD IN BLOOD OF SUBJECTS 1, 3, 5, 6 AND 9
Subject Rate of Change per Day Percentage of Airborne Lead in Blood
206pb/264pb
2d6pb/207pb
From 206Pb/204Pb
From 206Pb/207Pb
X io"4
X io"5
(Air)
17.60 ± 0.77
9.97 ± 0.42
1
• • •
0.70 ± 0.30
• • •
7 ± 3
3
5.52 ± 0.55
• • •
31.4 ± 3.4
• • •
5
• • •
3.13 ± 0.34
• • •
31.4 ± 3.7
6
6.53 ± 0.49
4.10 ± 0.25
37.1 ± 2.8
41.1 ± 3.0
9*
3.25
2.01
18.5
20.0
Note: Errors quoted are one standard deviation
*Frora slope of tangent drawn to the minima of subject's blood curves. Errors
cannot realistically be assigned.
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Stephens (1981) has extended the analysts of data in Manton's study (Table 11-55). He
used the observed air lead concentrations based on actual 24-hour air lead exposures in three
adults. He assumed values for breathing rate, lung deposition and absorption into blood to
estimate the blood lead uptake attributable to *04Pb by the direct inhalation pathway. Sub-
jects 5, 6 and 9 absorbed far more air lead in fact than was calculated using the values in
Table 11-54. The total air lead contribution was 8.4, 4.4 and 7.9 times larger than the
direct inhalation. These estimates are sensitive to the assumed parameter values.
In summary, the direct inhalation pathway accounts for only a fraction of the total air
lead contribution to blood, the direct inhalation contribution being on the order of 12 to 23
percent of the total uptake of lead attributable to gasoline, using Stephen's assumptions.
This is consistent with estimates (i.e. 8 to 54 percent) from the ILE study, taking into
account the much higher air lead levels in Turin.
11.5.1.2 Studies of Childhood Blood Lead Poisoning Control Programs. Billick et al. (1979)
presented several possible explanations for the observed decline in blood lead levels in New
York City children as well as evidence supporting and refuting each. The suggested contribu-
ting factors include the active educational and screening program of the New York City Bureau
of Lead Poisoning Control, and the decrease in the amount of lead-based paint exposure as a
result of rehabilitation or removal of older housing or changes in environmental lead exposure.
Information was only available to partially evaluate the last source of lead exposure and
particularly only for. ambient air lead levels. Air lead measurements were available during
the entire study period for only one station which was located on the west side of Manhattan
at a height of 56 m. Superposition of the air lead and blood lead levels indicated a
similarity in cycle and decline. The authors cautioned against overinterpretation by assuming
that one air monitoring site was representative of the air lead exposure of New York City
residents. With this in mind, the investigators fitted a multiple regression model to the
data to try to define the important determinants of blood lead levels for this population.
Age, ethnic group and air lead level were all found to be significant determinants of blood
lead levels. The authors further point out the possibility of a change in the nature of the
population being screened before and after 1973. They reran this regression analysis sepa-
rately for years both before and after 1973. The same results were still obtained, although
the exact coefficients varied.
Billick et al. (1980) extended their previous analysis of the data from the single moni-
toring site mentioned earlier. The investigators examined the possible relationship between
blood lead level and the amount of lead in gasoline used in the area. Figures 11-26 and 11-27
present illustrative trend lines in blood leads for blacks and Hispanics, vs. air lead and
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TABLE 11-55. CALCULATED BLOOD LEAD UPTAKE FROM AIR LEAD
USING MANTON ISOTOPE STUDY
Sub-
ject
Concen-
tration
Expo-
sure*
Deposi-
tion
Absorp-
tion
Blood Uptake from Air
Calcu-
lated
Inhala-
tion Observed
Fraction of lead
uptake from gasoline
by direct inhalation
5
0.22 Mg/m3
15 m^/day
37%
50%
0.61 pg/d
5.1 pfl/d
0.120
6
1.09 pg/m3
15 m3/day
37%
50%
3.0 pg/d
13.2 pg/d
0.229
9
0.45 pg/m3
3
15 m /day
37%
50%
1.2 pg/d
9.9 pg/d
0.126
*assumed rather than measured exposure, deposition and absorption.
Source: Stephens, 1981, based on Manton, 1977; Table III.
gasoline lead, respectively. Several different measures of gasoline lead were tried: aid-
Atlantic Coast (NY, NJ, Conn), New York, New York plus New Jersey and New York plus
Connecticut. The lead in gasoline trend line appears to fit the blood lead trend line better
than the air lead trend, especially in the summer of 1973.
Multiple regression analyses were calculated using six separate models. The best fitting
2
model had an R = 0.745. Gasoline lead content was included rather than air lead. The gaso-
line lead content coefficient was significant for all three racial groups. The authors state
a number of reasons for gasoline lead providing a better fit than air lead, including the fact
that the single monitoring site night not be representative.
Nathanson and Nude1man (1980) provide more detail regarding air lead levels in New York
City. In 1971, New York City began to regulate the lead content of gasoline sold. Lead in
gasoline was to be totally banned by 1974, but supply and distribution problems delayed the
effect of the ban. Ultimately regulation of lead in gasoline was taken over by the U.S.
Environmental Protection Agency.
New York City measured air lead levels during the periods June 1969 to September 1973 and
during 1978 at multiple sites. The earlier monitoring was done by 40 rooftop samples using
cellulose filters analyzed by AAS. The latter sampling was done by 27 rooftop samplers using
glass fiber filters analyzed by X-ray fluorescence (XRF). There was excellent agreement
between the XRF and atomic absorption analyses for lead (r = 0.985). Furthermore, the XRF
analyses were checked against EPA AAS and again excellent agreement was found. The authors
did, however, point out that cellulose filters are not as efficient as glass fiber filters.
Therefore, the earlier results tend to be underestimates of air lead levels.
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I I I | I I I | I I I | I I I | I I I | I I I | I I I
— — — HISPANIC
— • — AIR LEAD
2.0 >
1970
1971
1972
1973 1974 1975 1976
QUARTERLY SAMPLING DATE
Figure 11-26. Geometric mean blood lead levels of New York City
children (aged 25-36 months) by ethnic group, and ambient air lead
concentration versus quarterly sampling period, 1970-1976.
Source: Billick (1980).
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30
20
16
10
1 | 1 | I M | 1 I I | I I I | 1 I I | 1 I I [ I I I
BLACK
HISPANIC
QASOUNf LEAD
ns ' s
7 ^ X A
/ \ A I \ / t
\t \ I N/ \
A
W V/
A. / \ A V
^ ^ / \ / s/ \ / \
i# •. « • • *
\
V \
/V-
' / \ • \
v \/
so
S.0
4.0
3.0
>T 1 I I I 1 I I I I H I
1 I I I I I I 1 ton
1970 1971 1972 1973 1974 1978 1976
QUARTERLY SAMPLING DATE
Figure 11-27. Geometric mean blood lead levels of New York City
children (aged 28-38 months) by ethnic group, and estimated
amount of laad present in gasoline sold In New York, New Jersey,
and Connecticut versus quarterly sampling period, 1970-1976.
Source: Billick (1380).
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Quarterly citywide air lead averages generally declined during the years 1969-1978. The
3
maximum quarterly citywide average obtained was about 2.5 yg/m for the third quarter of 1970.
The citywide trend corresponds to the results obtained from the single monitoring site used in
Billick et al.'s analysis. The citywide data suggest that the single monitoring site in Man-
hattan is a responsible indicator of air lead level trends. The graph in Figure 11-28 rein-
forces this assertion by displaying the geometric mean blood lead levels for blacks and
Hispam*cs in the 25 to 36-month age groups and the quarterly citywide air lead levels for the
periods of interest. A good correspondence was noted.
As part of a detailed investigation of the relationship of blood lead levels and lead in
gasoline covering three cities, Billick (1982) extended the time trend analyses of New York
City blood lead data. Figure 11-29 presents the time trend line for geometric aean blood
leads for blacks age 24-35 months extended to 1979. The downward trend noted earlier was
still continuing, although the slopes for both the blood and gasoline lead seem to be somewhat
shallower toward the most recent data. A similar picture is presented by the percent of chil-
dren with blood lead levels greater than 30 Mg/dl- In the early 70's, about 60 percent of the
screened children had these levels; by 1979 the percent had dropped between 10 and 15 percent.
11.5.1.3 NHANES II. Blood lead data from the second National Health and Nutrition Examina-
tion Survey has been described in sections 11.3.3.1 and 11.3.4.4. The report by Annest et al.
(1983) found highly significant associations between amounts of lead used in gasoline produc-
tion in the U.S. and blood lead levels. The associations persisted after adjusting for race,
sex, age, region of the country, season, income and degree of urbanization.
Various analyses of the relationship between blood lead values in the NHANES II sample
and estimated gasoline lead usage were also reviewed by an expert panel (see Appendix 11-0).
They concluded that the correlation between gasoline lead usage and blood lead levels was con-
sistent with the hypothesis that gasoline lead is an important causal factor, but the analyses
did not actually confirm the hypothesis.
11.5.1.4 Frankfurt. West Germany. Sinn (1980; 1981) conducted a study specifically examining
the environmental and biological impact of the gasoline lead phasedown implemented in West
Germany on January 1, 1976. Frankfurt am Main provided a good setting for such a study
because of Its physical character.
Air and dustfall lead levels at several sites In and about the city were determined be-
fore and after the phasedown was Implemented. The mean air lead concentrations obtained
during the study are presented in Table 11-56. A substantial decrease in air lead levels was
noted for the low level high traffic site (3.18 pg/m3 in 1975-76 to 0.68 hS/h*3 1978-79).
No change was noted for the background site while only minor changes were observed for the
other locations. Oustfall levels fell markedly (218 itig/cm2• day for 1972-73 to 128 mg/cm2*day
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M I | 1 I I ) I II | I I I 1 II I | I I I | 1 I I
AIR LEAD
i
M
ftl»'»I '' 111111111111»11111111
1970 1171 1972 1973 1974 1976 1976
QUARTERLY SAMPLING DATE
Figure 11-28. Geometric mean Mood levels for blacks and
Hispanic* in the 25-to-36-montti ago group and rooftop
quarterly averages for ambient cltywide load (avals.
Source; Nathanson and Nudelman (1980).
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t
BO
i 40
8
1
1 »
a
o
e
a
§ 20
if
so-
ts
sF io
S3
aa
o
K 66 8788 8970 71 72 73 74 767677787980 81
YEAR
Figure 11-29. Time dependence of blood lead and gee lead for Macks, aged 24 to
3S months, in New York.
So *ce: Billlck (1882).
OEO. MEAN BLOOD Pt>
Source: Billick (1982).
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TABLE 11-56. MEAN AIR LEAD CONCENTRATIONS DURING THE VARIOUS BLOOD SAMPLING
PERIODS AT THE MEASUREMENT SITES DESCRIBED IN THE TEXT (pg/m3)
Residential High Traffic High Traffic Background
Low Traffic (>20m) (3m) Site
1975-1976 0.57 0.59 3.18 0.12
1976-1977 0.39 0.38 1.04 0.09
1977-1978 0.32 0.31 0.66 0.10
1978-1979 0.39 0.31 0.68 0.12
Source: Sinn (1980, 1981).
for 1977-78). Traffic counts were essentially unchanged in the area during the course of
study.
A number of population groups were Included in the study of the blood lead levels; they
were selected for having either occupational or residential exposure to high density automo-
bile traffic. Blood samples were taken serially throughout the study (three phases in
December-January 1975-76, December-January 1976-77 and December-January 1977-78). Blood
samples were collected by venipuncture and analyzed by three different laboratories. All the
labs used AAS although sample preparation procedures varied. A quality control program across
the laboratories was conducted. Due to differences in laboratory analyses, attrition and loss
of sample, the number of subjects who could be examined throughout the study was considerably
reduced from the initial number recruited (124 out of 300).
Preliminary analyses indicated that the various categories of subjects had different
blood lead levels, and that males and females within the same category differed. A very com-
plicated series of analyses then ensued that made it difficult to draw conclusions because the
various years' results were displayed separately by each laboratory performing the chemical
analysis and by different groupings by sex and category. In Sinn's later report (1981) a
downward trend was shown to exist for males and females who were in all years of the study and
whose blood levels were analyzed by the same laboratory.
11.5.2 Primary Smelters Populations
Most studies of nonindustry-employed populations living in the vicinity of industrial
sources of lead pollution were triggered because evidence of severe health impairment had been
found. Subsequently, extremely high exposures and high blood lead concentrations were found.
The following studies document the excessive lead exposure that developed, as well as some of
the relationships between environmental exposure and human response.
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11.5.2.1 El Paso, Texas. In 1972, the Centers for Disease Control studied the relationships
between blood lead levels and environmental factors in the vicinity of a primary smelter lo-
cated in El Paso, Texas emitting lead, copper and zinc. The smelter had been in operation
since the late 18001s (Landrigan et al., 1975; U.S. Centers for Oisease Control, 1973). Dally
1
Hi-Vol samples collected on 86 days between February and June 1972 averaged 6.6 Mg/m • These
air lead levels fell off rapidly with distance, reaching background values approximately S to
from the smelter. Levels were higher downwind, however. High concentrations of lead in soil
and house dusts were found, with the highest levels occurring near the smelter. The geometric
means of 82 soil and 106 dust samples from the sector closest to the smelter were 1791 and
4022 pg/g, respectively. Geometric means of both soil and dust lead levels near the smelter
were significantly higher than those in study sectors 2 or 3 km farther away.
Sixty-nine percent of children 1- to 4-years old living near the smelter had blood lead
levels greater than 40 pg/dl, and 14 percent had blood lead levels that exceeded 60 pg/dl.
Concentrations in older individuals were lower; nevertheless, 45 percent of the children 5- to
9-years old, 31 percent of the individuals 10- to 19-years old and 16 percent of the in-
dividuals above 19 had blood lead levels exceeding 40 pg/dl. The data presented preclude cal-
culations of means and standard deviations.
Data for people aged 1 to 19 years of age living near the smelter showed a relationship
between blood lead levels and concentrations of lead in soil and dust. For individuals with
blood lead levels greater than 40 the geometric mean concentration of lead in soil at
their homes was 2587 pg/g, whereas for those with a blood lead concentration less than 40
pg/dl, home soils had a geometric mean of 1419 pg/g. For house dust, the respective geometric
means were 6447 and 2067 pg/g. Length of residence was important only in the sector nearest
the smelter.
Additional sources of lead were also investigated. A relationship was found between
blood lead concentrations and lead release from pottery, but the number of individuals exposed
to lead-glazed pottery was very small. No relationships were found between blood lead levels
and hours spent out of doors each day, school attendance, or employment of a parent at the
smelter. The reported prevalence of pica also was minimal.
Data on dietary intake of lead were not obtained because there was no food available from
sources near the smelter since the climate and proximity to the smelter prevented any farming
in the area. It was unlikely that the dietary lead intakes of the children from near the
smelter or farther away were significantly different. It was concluded that the primary
factor associated with elevated blood lead levels in the children was Ingestion or inhalation
of dust containing lead.
Morse et al. (1979) conducted a follow-up investigation of the El Paso smelter to deter-
mine whether the environmental controls Instituted following the 1972 study had reduced the
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lead problem described. In November 1977, all children 1- to 18-years old living within
1.6 km of the smelter on the U.S. side of the border were surveyed. Questionnaires were ad-
ministered to the parents of each participant to gather background data.
Venous blood samples were drawn and analyzed for lead by modified Delves cup spectropho-
tometry. House dust and surface soil samples, as well as sample pottery items were taken from
each participant's residence. Dust and soil samples were analyzed for lead by AAS. Pottery
lead determinations were made by the extraction technique of Klein. Paint, food, and water
specimens were not collected because the earlier investigations of the problem had demon-
strated these media contributed little to the lead problem in El Paso.
Fifty-five of 67 families with children (82 percent) agreed to participate in the study.
There were 142 children examined in these homes. The homes were then divided into two groups.
Three children lived in homes within 0.8 km of the smelter. Their mean blood lead level in
1977 was 17.7 Mg/dl. By contrast, the mean blood lead level of 160 children who lived within
0.8 km of the smelter in 1972 had been 41.4 pg/dl. In 1977, 137 children lived in homes lo-
cated 0.8 to 1.6 km from the smelter. Their mean blood lead level was 20.2 pg/dl. The mean
blood level of 96 children who lived in that same area in 1972 had been 31.2 yg/dl.
Environmental samples showed a similar improvement. Dust lead fell from 22,191 pg/g to
I,479 pg/g while soil lead fell from 1,791 pg/g to 427 pg/g closest to the smelter. The mean
air lead concentration at 0.4 km from the smelter decreased from 10,0 to 5.5 pg/m3 and at 4.0
3
km from 2.1 to 1.7 pg/m . Pottery was not found to be a problem.
II.5.2.2 CDC-EPA Study. Baker et al. (1977b), in 1975, surveyed 1774 children 1 to 5 years
old, most of whom lived within 4 miles of lead, copper or zinc smelters located in various
parts of the United States. Blood lead levels were modestly elevated near 2 of the 11 copper
and 2 of the 5 zinc smelters. Although blood lead levels in children were not elevated in the
vicinity of three lead smelters, their FEP levels were somewhat higher than those found in
controls. Increased levels of lead and cadmium in hair samples were found near lead and zinc
smelters; this was considered evidence of external exposure. No environmental determinations
were made for this study.
11.5.2.3 Meza Valley, Yugoslavia. A series of Yugoslavian studies investigated exposures to
lead from a mine and a smelter in the Meza Valley over a period of years (Fugas et al., 1973;
Graovac-Leposavic et al. 1973; Milic et al., 1973; Djuric et al., 1971, 1972). In 1967,
24-hour lead concentrations measured on 4 different days varied fro* 13 to 84 jig/m^ in the
3
village nearest the smelter, and concentrations of up to 60 pg/m were found as far as 5 km
from the source. Mean particle size in 1968 was less than 0.8 pm. Analysis of some common
foodstuffs showed concentrations that were 10 to 100 times higher than corresponding food-
stuffs from the least exposed area (Meziea) (Djuric et al., 1971). After January 1969, when
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partial control of emissions was established at the smelter, weighted average weekly exposure
3
was calculated to be 27 pg/m in the village near the smelter. In contrast to this, the city
of Zagreb (Fugas et al., 1973), which has no large stationary source of lead, had an average
3
weekly air lead level of 1.1 pg/m .
In 1968, the average concentration of ALA In urine samples from 912 inhabitants of 6 vil-
lages varied by village from 9.8 to 13 mg/1. A control group had a mean ALA of 5.2 mg/1.
Data on lead 1n blood and the age and sex distribution of the villagers were not given (Djtiric
et al., 1971).
Of the 912 examined, 559 had an ALA level greater than 10 mg/1 of urine. In 1969, a more
extensive study of 286 individuals with ALA greater than 10 mg/1 was undertaken (Graovac-
Leposavic et al. 1973). ALA-U increased significantly from the previous year. When the
published data were examined closely, there appeared to be some discrepancies in inter-
pretation. The exposure from dust and from food might have been affected by the control de-
vices, but no data were collected to establish this. In one village, Zerjua, ALA-U dropped
from 21.7 to 9.4 mg/1 in children 2 to 7 years of age. Corresponding ALA-U values for 8- to
15-year-olds and for adult men and women were reduced from 18.7 to 12.1, from 23.9 to 9.9 and
from 18.5 to 9.0 mg/1, respectively. Because lead concentrations in air (Fugas et al., 1973),
even after 1969, indicated an average exposure of 25 pg/m , it is possible that some other
explanation should be sought. The author indicated in the report that the decrease in ALA-U
showed "the dependence on neteorologic, topographic, and technological factors" (Graovac-
Leposavlc et al., 1973).
Fugas (1977) in a later report estimated the time-weighted average exposure of several
populations studied during the course of this project. Stationary samplers as well as
personal monitors were used to estimate the exposure to airborne lead for various parts of the
day. These values were then coupled with estimated proportions of time at which these expo-
sure held. In Table 11-57, the estimated time-weighted air lead values as well as the ob-
served mean blood lead levels for these studied populations are presented. An increase in
blood lead values occurs with increasing air lead exposure.
11.5.2.4 Kosovo Province, Yugoslavia. Residents living in the vicinity of the Kosovo smelter
were found to have elevated blood lead levels (Popovac et al., 1982). In this area of
Yugoslavia, five air monitoring stations had been measuring air lead levels since 1S73. Mean
air lead varied from 7.8 to 21.7 pg/m3 In 1973; by 1980 the air lead averages ranged from 21.3
3
to 29.2 pg/m . In 1978 a pilot study suggested that there was a significant incidence of ele-
vated blood lead levels in children of the area. Two major surveys were then undertaken.
In August 1978 letters were sent to randomly selected families from the business commu-
nity, hospitals or lead-related industries in the area. All family members were asked to come
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TABLE 11-57. MEAN BLOOD LEAD LEVELS IN SELECTED YUGOSLAVIAN
POPULATIONS, BY ESTIMATED WEEKLY TIME-WEIGHTED AIR LEAD EXPOSURE
Population
N
Time-weighted,
air lead, nq/m
Blood lead level,
|jfl/dl SD
Rural I
49
0.079
7.9
4.4
Rural II
47
0.094
11.4
4.8
Rural III
45
0.146
10.5
4.0
Postmen
44
1.6
18.3
9.3
Customs officers
75
1.8
10.4
3.3
Street car drivers
43
2.1
24.3
10.5
Traffic policemen
24
3.0
12.2
5.1
Source: Fugas, 1977.
to a hospital for primary screening by erythrocyte protoporphyrin. A central population of
comparable socioeconomic and dietary background was collected fro* a town without lead emis-
sions. Blood levels were determined primarily for persons with greater than vq/g Mgb. EP was
measured by a hematof1uorimeter, while blood lead was determined by the method of Fernandez
using atomic absorption with graphite furnace and background correction.
Mean EP values were higher in the 1978 survey for exposed residents compared to controls
in the average age group. EP values seemed to decline with age. Similar differences were
noted for blood lead levels. The observed mean blood leads, ranging from 27.6 in the greater
than 15-year age group to 50.9 |jg/dl in the 5- to 10-year group, suggest substantial lead ex-
posure of these residents. In the control group the highest blood lead level was 19 Mfl/dl•
In December 1980 a second survey was conducted to obtain a more representative sample of
persons residing in the area. Letters were sent again, and 379 persons responded. EP levels
were higher in all ages in 1980 vs. 1978, although the differences were not statistically sig-
3 3
nificant. The air lead levels Increased from 14.3 m9/« in 1978 to 23.8 yg/m 1n 1980.
Comparing the 1980 blood lead results with the 1978 control group shows that the 1980
levels were higher in each age group. Males older than 15 years had higher mean blood lead
levels than the females (39.3 vs. 32.4 pg/dl).
11.5.2.5 The Cavallerl Study. Cavalleri et al. (1981) studied children In the vicinity of a
lead smelter and children from a control area (4 km from the smelter). The exposed population
consisted of 85 children aged 3 to 6 attending a nursery school and 80 primary school children
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aged 8 to 11. The control population was 25 nursery school children aged 3 to 6 and 64 pri-
mary school children aged 8 to 11. Since the sue "Iter had installed filters 8 years before the
study, the older children living in the smelter area had a much higher lifetime exposure.
Blood lead analysis was performed on venous samples using anodic stripping voltamnetry by
Worrell's method. Precision was checked over the range 10 to 100 (jg/dl. Reported reproduci-
bility was also good. All samples were subsequently reanalyzed by AAS using graphite furnace
and background correction by the method of Volosen. The average values obtained by the
second method were quite similar to those of the first (average difference 1.4 yg/dl; cor-
relation coefficient, 0.962).
Air was sampled for lead for 1 month at three sampling sites. The sites were located at
ISO m, 300 in and 4 km from the wall of the lead smelter. The average air lead levels were
3
2.32, 3.43 and 0.56 pg/m , respectively.
A striking difference in blood lead levels of the exposed and control populations was ob-
served; levels in the exposed population were almost twice that in the control population.
There was no significant difference between nursery school and primary school children. The
geometric mean for nursery school children was 15.9 and 8.2 for exposed and control, respecti-
vely/ For primary school it was 16.1 and 7.0 Mfl/dl ¦ In the exposed area 23 percent of the
subjects had blood lead levels between 21 and 30 and 3 percent greater than 31 vg/
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Blood leads were statistically significantly higher closer to the swelter. For all chil-
dren the nean blood lead level was 19.7 yg/dl for the less than 1 In and 11.8 |jg/dl for the
controls (>2 km). Similarly, FEP levels were higher for the closer (41,9 pg/100 ml RBC)
children as opposed to the control (32.5 ng/100 Ml R8C). Higher blood levels were associated
with lower socioeconomic status.
Further Investigation of this smelter was undertaken by Brunekreef et al. (1981) and
Diemel et al. (1981). In May 1978 venipuncture blood samples were collected from 95 one- to
three-year old children living within 1 km of the smelter. Blood leads were determined by
graphite AAS.
Before the blood sampling, an environmental sampling program was conducted. The samples
collected are listed in Table 11-58. Questionnaires were administered to collect background
and further exposure information. A subset of 39 children was closely observed for 1 or 2
days for mouthing behavior. Table 11-58 also presents the overall results of the environ-
mental sampling. As can be readily seen, there is a low exposure to airborne lead (G.N.
3 3
0.41 Mg/» with a range of 0.28 to 0.52 yg/m ). Soil exposure was moderate, although high.
Interior dust was high in lead, geometric mean of 967 yg/g with a maximum of 4741 Mg/fl- In *
few homes, high paint lead levels were found. Diemel et al. (1981) extended the analysis of
the environmental samples. They found that indoor pollution was lower than outside. In
Arnhem, it was found that lead is carried into the homes in particulate form by sticking to
shoes. Most of the lead originated from soil from gardens and street dust.
Simple correlation coefficients were calculated to investigate the relationship between
log blood lead and the independent variables. Significantly, correlations were found with
quantity of house dust, quantity of deposited lead indoors, observational score of dustiness,
age of child and the average number of times an object is put in the mouth. Multiple regre-
ssion analyses were calculated on four separate subpopulations. Among children living in
houses with gardens, the combination of soil lead level and educational level of the parents
explained 23 percent of the variations of blood lead. In children without gardens, the amount
of deposited lead indoors explained 26 percent of the variarice. The authors found that an
increase in soil lead level from 100 to 600 pg/g results in an increase In blood lead of
63 pg/dl.
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TABLE 11-58. ENVIRONMENTAL PARAMETERS AND METHODS: ARNHEM LEAD STUDY, 1978a
Parameter Method Geometric Mean Range
1.
Lead in.ambient air
(pg/«0
High volume samples; 24-hr measurements
at 6 sites, continuously for 2 months
0.41
0.28-0.52
2.
Lead in-dustfall
(pg/m -day)
Standard deposit gauges; 7-day measurements
at 22 sites, semlcontinuously for 3 months
467
108-2210
3.
Lead 1n soil
Sampling in gardens of study populations;
analysis of layers from 0 to 5 cm and
5 to 20 cm
240
21-1126
4.
Lead in street dust
(H9/fl)
Samples at 31 sites, analysis of fraction
<0.3am
690
77-2667
5.
Lead in,indoor air
(fig/m )
Low volume samples; 1-month measurements
in homes of study population, continuously
for 2 months
0.26
0.13-0.74
6.
Lead in dustfall
indoors (pg/n -day)
Greased glass plates of 30 x 40 cm; 1-month
measurements in homes of study population,
continuously for 3 months
7.34
1.36-42.35
7.
Lead in floor dust
(M8/g)
Vacuum cleaner with special filter
holder; 5 samples, collected on 3 different
occasions; with intervals of approximately
1 month, in homes of study populations
fine 957
course 282
463-4741
117-5250
8.
Easily available
lead indoors
Wet tissues, 1 sample in homes of study
population
85% of samples
<20 MS Pb/tissue
9.
Lead in tapwater
Proportional samples, during 1 week in
homes of study population
5.0 (arthimetic)
mean
<0.5-90.0
10.
Dustiness of homes
Visual estimation, on a simple scale ranging
from 1 (clean) to 3 (dusty); 6 observations
in homes of study population
All lead analyses were perforaed by atonic absorption spectrophotometry, except part of the tapwater analysis
which was perforaed by anodic stripping voltametry. Lead in tapwater analyzed by the National Institute of
Drinking Water Supply in Leidscherdam. Soil and street dust analyzed by the Laboratory of Soil and Plant
Research in Oosterbeek. (Zielhuis, et. al., 1979; Diemel, et. al., 1981)
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11.5.4 Secondary Swelters
In a Dallas, Texas, study of two secondary lead smelters, the average blood lead levels
of exposed children was found to be 30 pg/dl vs. an average of 22 pg/dl in control children
(Johanson and Luby, 1972). For the two study populations, the air and soil lead levels were
3.5 and 1.5 pg/m3 and 727 and 255 pg/g, respectively.
In Toronto, Canada the effects of two secondary lead smelters on the blood and hair lead
levels of nearby residents have been extensively studied (Ontario Ministry of the Environment,
1975; Roberts et al., 1974). In a preliminary report, Roberts et al. (1974) stated that blood
and hair lead levels were higher 1n children living near the two smelters than in children
living 1n an urban control area. Biologic and environmental lead levels were reported to de-
crease with increasing distance from the base of the smelter stacks.
A later and more detailed report Identified a high rate of lead fallout around the two
secondary smelters (Ontario Ministry of the Environment, 1975). Two groups of children living
within 300 if of each of the smelters had geometric mean blood lead levels of 27 and 28 pg/dl,
respectively; the geometric mean for 1231 control^, was 17 pg/dl. Twenty-eight percent of the
sample children tested near one smelter during the summer and 13 percent of the sample chil-
dren tested near the second smelter during the winter had blood lead levels greater than 40
pg/dl. Only 1 percent of the controls had blood lead levels greater than 40 pg/dl. For chil-
dren, blood lead concentrations increased with proximity to both smelters, but this trend did
not hold for adults, generally. The report concluded that soil lead levels were the main de-
terminant of blood lead levels; this conclusion was disputed by Horn (1976).
Blood lead levels 1n 293 Finnish individuals, aged 15 to 80, were significantly cor-
related with distance of habitation from a secondary lead smelter (Nordman et al., 1973). The
geometric mean blood lead concentration for 121 males was 18.1 (jg/dl; for 172 females, 1t was
14.3 pg/dl. In 59 subjects who spent their entire day at home, a positive correlation was
found between blood lead and distance from the smelter up to 5 km. Only one of these 59 in-
dividuals had a blood lead greater than 40 pg/dl, and none exceeded 50 pg/dl.
11.5.5 Secondary Exposure of Children
Excessive Intake and absorption of lead on the part of children can result when parents
who work in a dusty environment with a high lead content bring dust home on their clothes,
shoes or even their automobiles. Once they are home, their children are exposed to the dust.
Landrlgan et al. (1976) reported that the 174 children of smelter workers who lived with-
in 24 km of the smelter had significantly higher blood lead levels, a mean of 55.1 than
the 511 children of persons in other occupations who lived in the same areas whose mean
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blood lead levels were 43.7 jjg/dl. Analyses by EPA of the data collected in Idaho showed that
employment of the father at a lead smelter, at a zinc smelter, or in a lead nine resulted in
higher blood lead levels in the children living in the same house as opposed to those children
whose fathers were employed in different locations (Table 11-59). The effect associated with
parental employment appears to be much more prominent in the most contaminated study areas
nearest to the smelter. This may be the effect of an intervening socioeconomic variable: the
lowest paid workers, employed in the highest exposure areas within the industry, might be ex-
pected to live in the most undesirable locations, closest to the smelter.
TABLE 11-59. GEOMETRIC MEAN BLOOD LEAD LEVELS FOR CHILDREN
BASED ON REPORTED OCCUPATION OF FATHER, HISTORY
OF PICA, AND DISTANCE OF RESIDENCE FROM SMELTER
Lead
smelter Lead/zinc mine Zinc smelter Other
worker worker worker occupations
Area
from
smelter, km
Pica
No
Pica
Pica
No
Pica
Pica
No
Pica
Pica
No
Pica
1
1.6
78.7
74.2
75.3
63.9
69.7
59.1
70.8
59.9
2
1.6 to 4.0
50.2
52.2
46.9
46.9
62.7
50.3
37.2
46.3
3
4.0 to 10.0
33.5
33.3
36.7
33.5
36.0
29.6
33.3
32.6
.4
10.0 to 24.0
-
30.3
38.0
32.5
40.9
36.9
-
39.4
5
24.0 to 32.0
-
24.5
31.8
27.4
-
-
28.0
26.4
6
75
-
-
-
-
-
-
17.3
21.4
Source: Landrigan et al. 1976.
Landrigan et al. (1976) also reported a positive history of pica for 192 of the 919 chil-
dren studied 1n Idaho. This history was obtained by physician and nurse interviews of
parents. Pica was most common among 2-year old children and only 13 percent of those with
pica were above age 6. Higher blood lead levels were observed in children with pica than in
those without pica. Table 11-59 shows the mean blood lead levels in children as they were af-
fected by pica, occupation of the father and distance of residence from the smelter. Among
the populations living nearest to the smelter environmental exposure appears to be sufficient
at times to more than overshadow the effects of pica, but this finding may also be caused by
Inadequacies inherent in collecting data on pica.
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These data Indicate that in a heavily contaminated area, blood lead levels in children
¦ay be significantly increased by the intentional ingestion of nonfood materials having a high
lead content.
Data on the parents' occupation are, however, more reliable. It must be remenbered also
that the study areas were not homogeneous socioeconomically. In addition, the specific type
of work an individual does in an industry is probably much more important than simply being
employed in a particular Industry. The presence in the home of an industrial employee exposed
occupational ly to lead may produce Increases 1n the blood lead levels ranging from 10 to 30
percent.
The importance of the infiltration of lead dusts onto clothing, particularly the under-
garments, of lead workers and their subsequent transportation has been demonstrated in a
number of studies on the effects of smelters (Martin et al., 1975). It was noted in the
United Kingdom that elevated blood lead levels were found in the wives and children of
workers, even though they resided some considerable distance from the facility. It was most
prominent in the workers themselves who had elevated blood lead levels. Quantities of lead
dust were found in workers' cars and homes. It apparently is not sufficient for a factory
merely to provide outer protective clothing and shower facilities for lead workers. In
another study in Bristol, from 650 to 1400 pg/g of lead was found in the undergarments of
workers as compared with 3 to 13 pg/g in undergarments of control subjects. Lead dust will
remain on the clothing even after laundering: up to 500 mg of lead has been found to remain
on an overall garment after washing (Lead Development Association, 1973).
Baker et al. (1977a) found blood lead levels greater than 30 pg/dl In 38 of 91 children
whose fathers were employed at a secondary lead smelter in Memphis, TN, House dust, the only
source of lead 1n the homes of these children, contained a mean of 2687 nfl/fl compared with 404
Mg/g in the homes of a group of matched controls. Mean blood lead levels in the workers'
children were significantly higher than those for controls and were closely correlated with
the lead content of household dust. In homes with lead in dust less than 1000 jig/g, 18 chil-
dren had a mean blood lead level of 21.8 ± 7.8 Mg/dl, whereas 1n homes where lead 1n dust was
greater than 7000 pg/fl. 6 children had mean blood lead levels of 78.3 ± 34.0 pg/dl. See
Section 7.3.2.1.6 for a further discussion of household dust.
Other studies have documented increased lead absorption in children of families where at
least one member was occupationally exposed to lead (Fischbein et al., 1980a). The occupa-
tional exposures involved battery operations (Morton et al., 1982; U.S. Centers for Disease
Control, 1977b; Dolcourt et al., 1978, 1981; Watson et al., 1978; Fergusson et al., 1981) as
well as other occupations (Snee, 1982b; Rice et al., 1978).
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In late summer of 1976, a battery plant in southern Vermont provided the setting for the
first documented instance of increased lead absorption in children of employees in the battery
industry. The data were first reported by U.S. Centers for Disease Control (1977b) and more
completely by Watson et al. (1978).
Reports of plant workers exposed to high levels of lead stimulated a study of plant
employees and their children in August and September 1975. In the plant, lead oxide powder is
used to coat plates in the construction of batteries. Before the study, the work setting of
all 230 employees of the plant had been examined and 62 workers (22 percent) were identified
as being at risk for high lead exposure. All of the high risk workers interviewed reported
changing clothes before leaving work and 90 percent of them reported showering. However, 87
percent of them stated that their work clothes were washed at home.
Of the high risk' employees, 24 had children between the ages of 1 and 6 years. A case-
control study was conducted in the households of 22 of these employees. Twenty-seven children
were identified. The households were matched with neighborhood controls including 32 control
children. None of the control family members worked in a lead industry. Capillary blood
specimens were collected from all children and the 22 battery plant employees had venous spec-
imens taken. All blood samples were analyzed for lead by AAS. Interviewers obtained back-
ground data, including an assessment of potential lead exposures.
About 56 percent of the employees' children had blood leads greater than 30 pg/d1 com-
pared with about 13 percent of the control children. Mean blood lead levels were stat-
istically significantly different, 31.8 M9/dl and 21.* pg/dl, respectively. Blood lead levels
in children were significantly correlated with employee blood lead levels.
House dust lead levels were measured in all children's homes. Mean values were 2239.1
pg/g and 718.2 nfl/fl for employee and control homes, respectively; this was statistically sig-
nificant. Examination of the correlation coefficient between soil lead and blood lead levels
1n the two sets of homes showed a marginally significant coefficient 1n the employee household
but no correlation in the control homes. Tap water and paint lead levels did not account for
the observed difference 1n blood leads between children of workers and neighborhood controls.
It is significant that these findings were obtained despite the changing of clothes at the
plant.
Morton et al. (1982) conducted their study of children of battery plant workers and con-
trols during February-March 1978. Children were included in the study 1f one parent had at
least 1 year of occupational exposure, 1f they had lived at the same residence for at least 6
months, and if they were from 12-83 months of age. Children for the control group had to have
no parental occupational exposure to lead for 5 years, and had to have lived at the same ad-
dress at least 6 months.
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Thirty-four children were control matched to the exposed group by neighborhoods and age
(±1 year). No Batching was thought necessary for sex because In this age group blood lead
levels are unaffected by sex. The selection of the control population attempted to adjust for
both socioeconomic status as well as exposure to automotive lead.
Capillary blood specimens were collected concurrently for each matched pair. Blood lead
levels were measured by the CDC lab using a modified Delves cup AAS procedure. Blood lead
levels for the employees for the previous year were obtained from company records. Question-
naires were administered at the same time as the blood sampling to obtain background informa-
tion. The homemaker was asked to complete the interview to try to get a more accurate picture
of the hygiene practices followed by the employees.
Children's blood lead levels differed significantly between the exposed and control
groups. Fifty-three percent of the employees' children had blood lead levels greater than 30
Hfl/dl, while no child in the control population had a value greater than 30 pg/dl. The mean
blood lead for the children of the employees was #9.2 pg/dl with a standard deviation of 8.3
fjg/dl. These data represent the population average for yearly individual average levels. The
employees had an average greater than 60 pg/dl. Still, this is lower than the industry
average. Of the eight children with blood levels greater than 40 pg/dl, seven had fathers
with blood lead greater than 50 §jg/dl- Yet there was not a significant correlation between
children's blood lead level and father's blood lead level.
Investigations were made into the possibility that other lead exposures could account for
the observed difference in blood lead levels between children of employees and control chil-
dren. In 11 of the 33 pairs finally Included in the study, potential lead exposures other
than fathers' occupations were found in the employee child of the matched pair. These in-
cluded a variety of lead sources such as automobile body painting, casting of lead, and
playing with spent shell casings. The control and exposed populations were again compared
after removing these 11 pairs from consideration. There was still a statistically significant
difference in blood lead level between the two groups of children.
An examination of personal hygiene practices of the workers showed that within high ex-
posure category jobs, greater compliance with recommended lead containment practices resulted
' in lower mean blood lead levels in children. Mean blood leads were 17.3, 36.0 and 41.9 pg/dl
for good, moderately good and poor compliance groups, respectively. In fact, there was only a
small difference between the good hygiene group within the high exposure category and the mean
of the control group (17.3 |jg/d1 vs. 15.9 Mfl/dl). Insufficient sample sizes were available to
evaluate the effect of compliance on medium and low lead exposures for fathers.
Oolcourt et al. (1978) Investigated lead absorption in children of workers in a plant
that manufactures lead-acid storage batteries. The plant became known to these researchers as
a result of finding an elevated blood lead level in a 20-month-old child during routine
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screening. Although the child was asymptomatic, his mother proved not to be. Two siblings
were also found to have elevated blood lead levels. The .mother was employed by the plant; her
work involved much hard labor and brought her into continual contact with powdery lead oxide.
No uniforms or garment covers were provided by the company. As a result of these findings,
screening was offered to all children of plant employees.
During February to May 1977, 92 percent of 63 eligible children appeared for screening.
Age ranged from 10 months to 15 years. About equal numbers of girls and boys underwent
screening. Fingerstick blood samples were collected on filter paper and were analyzed for
lead by AAS. Children with blood lead levels equal to or greater than 40 jjg/dT were referred
for more detailed medical evaluation including an analysis of a venous blood specimen for
lead. Dust samples were collected from carpeting in each home and analyzed for lead by gra-
phite furnace AAS. Home tap water was analyzed for lead by AAS, and house paint was analyzed
for lead by XRF.
Of the 58 children who had the initial fingerstick blood lead elevation, 69 percent had
blood lead levels equal to or greater than 30 pg/dl. Ten children from six families had blood
lead levels equal to or greater than 40 pg/dl, and blood lead levels were found to vary
markedly with age. The 0- to 3-year old category exhibited the highest mean with the 3- to
6-year-olds the next highest (39.2 pg/dl). Lowest mean values were found in the equal to or
greater than 10-year-old group (26.7 pg/dl).
More detailed investigation of the six families with the highest blood lead levels in
their children revealed the following: five of the six lived in rural communities, with no
pre-existing source of lead from water supply, house paint, industrial emissions or heavy
automobile traffic. However, dust samples from the carpets exhibited excessively high lead
concentrations. These ranged from 1700 to 84,050 pg/g.
Fergusson et al. (1981) sampled three population groups: general population, employees
of a battery plant, and children of battery plant employees, using hair lead levels as indices
of lead. Hair lead levels ranged from 1.2 to 110.9 pg/g in the 203 samples from the general
population. The distribution of hair lead levels was nearly lognormal. Employees of the bat-
tery factory had the highest hair lead levels (median ~250 pg/g) while family members (median
~40 MS/g) had a lesser degree of contamination and the general population (median ~5 pg/g)
still less.
Analysis of variance results indicated a highly significant difference between mean lead
levels of the general survey and family members of the employees, and a significant difference
between the mean lead levels in the hair of the employees and their families. No significant
differences were found comparing mean hair lead levels among family members in terms of age
and sex. The analyses of the house dust suggested that the mechanism of exposure of family
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¦embers Is via the lead in dust that is carried home. Mean dust lead levels among the hones
of factory employees was 5580 pg/g while the dust inside of houses along a busy road was only
1620 Mfl/fl- Both of these concentrations are for particles less than 0.1 am.
Dolcourt et al. (1981) reported two interesting cases of familiar exposure to lead caused
by recycling of automobile storage batteries. The first case was of a 22 member, 4 generation
family living in a three bedroom house in rural eastern North Carolina. The great grandfather
of the index case worked at a battery recycling plant. He had two truck!oads of spent casings
delivered to the home to serve as fuel for the wood stove; the casings were burned over a 3-
month period.
The index case presented with classic signs of acute lead encephalopathy, the most severe
and potentially fatal form of acute lead poisoning. The blood lead level was found to be 220
Mg/dl. Three months after initial diagnosis and after chelation therapy, she continued to
have seizures and was profoundly mentally retarded. Dust samples were obtained by vacuum
cleaner and analyzed for lead by flameless AAS. Dust from a sofa near the wood stove con-
tained 13,283 lead while the kitchen floor dust had 41,283 Mfl/fl- There was no paint
lead. All other members of the family had elevated blood lead levels ranging from 27-256
Mg/dl.
The other case involved a truck driver working 1n a low exposure area of a battery re-
cycling operation in rural western North Carolina. He was operating an illegal battery re-
cycling operation in his home by melting down reclaimed lead on the kitchen stove. No family
member was symptomatic for lead symptoms but blood lead levels ranged from 24 to 72 jjg/dl.
Soil samples taken from the driveway, which was paved with fragments of the discarded battery
casing, contained 12-13 percent lead by weight.
In addition to families being exposed as a result of employment at battery plants, stu-
dies have been reported recently for smelter worker families (Rice et al., 1978; Snee, 1982c).
Rice et al. studied lead contamination in the homes of secondary lead smelters. Homes of em-
ployees of secondary smelters in two separate geographic areas of the country were examined to
determine whether those homes had a greater degree of lead contamination than homes of workers
in the same area not exposed to lead. Both sets of homes ( area I and II) were examined at
the same time of the year.
Thirty-three homes of secondary smelter employees were studied; 19 homes in the same or
similar neighborhoods were studied as controls. Homes studied were in good condition and were
one or two family dwellings. Blood lead levels were not obtained for children 1n these homes.
In the hones of controls, a detailed occupational history was obtained for each employed
person. Homes where one or more residents were employed in a lead contaminated environment
were excluded from the analysis.
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House dust samples were collected by Vostal's method and were analyzed for lead by AAS.
In one of the areas, samples of settled dust were collected from the homes of employees and
controls. Dust was collected over the doorways. In homes where the settled dust was col-
lected, zinc protoporphyrin (ZPP) determinations were made in family members of the lead
workers and in the controls.
In both areas the wipe samples were statistically significantly higher in the homes of
employees compared to controls (geometric mean 79.3 ± 61.8 pg/g vs. 28.8 ± 7.4 pg/g Area I;
112.0 ± 2.8 pg/g vs. 9.7 ± 3.9 pg Area II). No significant differences were found between
workers' homes or controls between Area I and Area II. Settled dust lead was significantly
higher in the homes of employees compared to controls (3300 vs. 1200 pg/g). Lead content of
particulate matter collected at the curb and of paint chips collected in the home was not sig-
nificantly different between employee homes and controls. Zinc protoporphyrin determinations
were done on 15 children, 6 years or younger. ZPP levels were higher in employee children
than 1n control children. Mean levels were 61.4 pg/ml and 37.6 pg/ml, respectively.
It should be noted again that the wipe samples were not different between employee homes
1n the two areas. Interviews with employees Indicated that work practices were quite similar
1n the two areas. Most workers showered and changed before going home. Work clothes were
washed by the company. Obviously much closer attention needs to be paid to other potential
sources of lead introduction into the home (e.g., automobile surfaces).
11.5.6 Miscellaneous Studies
11.5.6.1 Studies Using Indirect Measures of Air Exposure.
11.5.6.1.1 Studies in the United States. A 1973 Houston study examined the blood lead levels
of parking garage attendants, traffic policemen, and adult females living near freeways
(Johnson et al., 1974). A control group for each of the three exposed populations was selec-
ted by matching for age, education and race. Unfortunately, the matching was not altogether
successful; traffic policemen had less education than their controls, and the garage employees
were younger than their controls. Females were matched adequately, however. It should be
noted that the mean blood lead values for traffic policemen and parking garage attendants, two
groups regularly exposed to higher concentrations of automotive exhausts, were significantly
higher than the means for their relevant control groups. Statistically significant dif-
ferences 1n mean values were not found, however, between women living near a freeway, and con-
trol women living at greater distances from the freeway.
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A study of the effects of lower level urban traffic densities on blood lead levels was
undertaken in Dallas, Texas, in 1976 (Johnson et al., 1978). The study consisted of two
phases. One phase measured air lead values for selected traffic densities and conditions,
ranging from equal to or less than 1,000 to about 37,000 cars/day. The second phase consisted
of an epidemiological study of traffic density and blood lead levels among residents. Figure
11-30 shows the relationship between arithmetic means of air lead and traffic density. As can
be seen from the graph, a reasonable fit was obtained.
In addition, for all distances measured (1.5 to 30.5 m from the road), air lead concen-
trations declined rapidly with distance from the street. At 15 m, concentrations were about
55 percent of the street concentrations. In air lead collections from 1.5 to 30.5 a from the
street, approximately 50 percent of the airborne lead was in the respirable range (<1 pm), and
the proportions in each size class remained approximately the same as the distance from the
street increased.
Soil lead concentrations were higher in areas with greater traffic density, ranging from
73.6 |jg/g at less than 1,000 cars per day to a mean of 105.9 at greater than 19,500 cars per
day. The maximum soil level obtained was 730 HO/fl-
Dustfal1 samples for 28 days from 9 locations showed no relationship to traffic
densities, but outdoor levels were at least 10 times the indoor concentration in nearby
residences.
In the second phase, three groups of subjects, 1- to 6-years-old, 18- to 49-years old and
50 years and older, were selected in each of four study areas. Traffic densities selected
were less than 1,000, 8,000 to 14,000, 14,000 to 20,000 and 20,000 to 25,000 cars/day. The
study groups averaged about 35 subjects, although the number varied from 21 to 50. The
smallest groups were from the highest traffic density area. No relationship between traffic
density and blood lead levels in any of the age groups was found (Figure 11-31). Blood lead
levels were significantly higher in children, 12 to 18 M9/d1. than in adults, 9 to 14 jig/dl.
Gaprio et al. (1974) compared blood lead levels and proximity to major traffic arteries
in a study reported In 1971 that included 5226 children in Newark, New Jersey. Over 57 per-
cent of the children living within 30.5 m of roadways had blood lead levels greater than 40
Mfl/dl. For those living between 30.5 and 61 m from the roadways, more than 27 percent had
such levels, and at distances greater than 61 m, 31 percent exceeded 40 ng/dl. The effect of
automobile traffic was seen only in the group that lived within 30.5 m of the road.
No other sources of lead were considered in this study. However, data from other studies
on mobile sources indicate that it is unlikely that the blood lead levels observed in this
study resulted entirely from automotive exhaust emissions.
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Y = 0.8698 + 0.0263 X
X - TRAFFIC COUNT/1000
J I 1 I I I I ' »
0 4,000 8,000 12,000 16,000 20,000 24,000 28,000 32,000 36,000 38,000
TRAFFIC VOLUME, cara/day
Figure 11-30. Arithmetic mean of air lead levels by traffic volume,
Dallas, 1976.
In 1864, Thomas et al. (1967) Investigated blood lead levels in 50 adults who had lived
for at least 3 years within 76 a of a freeway (Los Angeles) and those of 50 others who had
lived for a similar period near the ocean or at least 1.6 km from a freeway. Mean blood lead
levels for those near the freeway were 22.7 ±5.6 for men and 16.7 ±7.0 pg/dl for women.
These concentrations were higher than for control subjects living near the ocean: 16.0 ± 8.4
pg/dl for men and 9.9 ±4.9 nfl/dl for women. The higher values, however, were similar to
those of other Los Angeles populations. Measured mean air concentrations of lead in Los
Angeles for October 1964 were 12,25 ± 2.70 Hg/m3 at a location 9 n» from the San Bernardino
freeway; 13.25 ± 1.90 mq/i*3 at a fourth floor location 91.5 m from the freeway; and 4.60 ±
1.92 pg/m3 1.6 km from the nearest freeway. The investigators concluded that the differences
observed were consistent with coastal inland atmospheric and blood lead gradients in the Los
Angeles basin and that the effect of residential proximity to a freeway (7.6 to 76 a) was not
demonstrated.
Ter Haar and Chadzynski report a study of blood lead levels of children living near three
heavily travelled streets in Detroit (Ter Haar, 1981; Ter Haar and Chadzynski, 1979). Blood
lead levels were not found to be related to distance from the road but were related to condi-
tions of housing and age of the child after multiple regression analyses.
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25
20
IS
10
// \ FEMALES <9
/ £» V
MALES <9
•O — -
MALES >49
FEMALES 19-48
rrs
FEMALES >49
_L
_L
<1,000 1,000-13,500 13,500- 19,500-
19,500 38,000
TRAFFIC DENSITY, cars/day
Figure 11-31. Blood lead concentration and traffic density by sex and
age, Dallas, 1978.
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11.5.6.1.2 British Studies. In a Birmingham, England study, mean blood lead levels in 41
males and 58 females living within 800 m of a highway interchange were 14.41 and 10.93 MS/dl.
respectively, just before the opening of the interchange in May 1972 (Waldron, 1975). From
October 1972 to February 1973, the respective values for the same individuals were 18.95 and
14.93 (jg/dl. In October 1973 they were 23.73 and 19.21 ng/dl¦ The Investigators noted dif-
ficulties in the blood collection method during the baseline period and changed from capillary
to venous blood collection for the remaining two samples. To interpret the significance of
the change in blood collection method, some individuals gave both capillary and venous blood
at the second collection. The means for both capillary and venous bloods were calculated for
the 18 males and 23 females who gave both types of blood samples (Barry, 1975). The venous
blood mean values for both these males and females were lower by 0.8 and 0.7 pg/dl, respec-
tively. If these differences were applied to the means of the third series, the mean for
males would be reduced to 24.8 pg/dl and that for the females to 18.7 jjg/dl. These adjusted
means still show an increase over the means obtained for the first series. Comparing only the
means for venous bloods, namely series two and three, again shows an increase for both groups.
The increase in blood lead values was larger than expected following the model of Knelson et
al. (1973), because air lead values near the road were approximately 1 ng/m3. The investi-
gators concluded that either the lead aerosol of very small particles behaved more like a gas
so that considerably more than 37 percent of inhaled material was absorbed or that ingestion
of lead contaminated dust might be responsible.
Studies of taxi cab drivers have employed different variables to represent the drivers'
lead exposure (Flindt et al., 1976; Jones et al., 1972): one variable was night vs. dayshift
drivers {Jones et al., 1972); the other, mileage driven (Flindt et al., 1976). No difference
was observed, in either case.
The studies reviewed show that automobiles produce sufficient emissions to increase air
and nearby soil concentrations of lead as well, as increase blood lead concentrations in chil-
dren and adults. The problem is of greater importance when houses are located within 100 ft
(30 m) of the roadway.
11.5.6.2 Miscellaneous Sources of lead. The habit of cigarette smoking is a source of lead
exposure. Shaper et al. (1982) report that blood lead concentration is higher for smokers
than nonsmokers and that cigarette smoking makes a significant independent contribution to
blood lead concentration in middle-aged men in British towns. A direct increase in lead in-
take from cigarettes is thought to be responsible. Hopper and Mathews (1983) comnent that
current smoking has a significant effect on blood lead level, with an average increase of 5.8
percent in blood lead levels for every 10 cigarettes smoked per day. They also report that
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past smoking history had no measurable effect on blood lead levels. Hasselblad and Nelson
(1975) report an average increase in women's blood lead levels of 1.3 pg/dl in the study of
Tepper and Levin (1975).
Although no studies are available, it is conceivable that destruction of lead-containing
plastics (to recover copper), which has caused cattle poisoning, also could become a source of
lead exposure for humans. Waste disposal is a more general problem because lead-containing
materials may be Incinerated and may thus contribute to increased air lead levels. This
source of lead has not been studied in detail. Tyrer (1977) cautions of the lead hazard in
the recycling of waste.
The consumption of illicitly distilled liquor has been shown to produce clinical cases of
lead poisoning. Domestic and imported earthenware (De Rosa et a!., 1980) with improperly
fired glazes have also been related to clinical lead poisoning. This source becomes important
when foods or beverages high 1n acid are stored in earthenware containers, because the add
releases lead from the walls of the containers.
Particular cosmetics, popular among some Oriental and Indian ethnic groups, contain high
percentages of lead that sometimes are absorbed by users in quantities sufficient to be toxic.
Ali et al. (1978) and Attenburrow et al. (1980) discuss the practice of surma and lead poison-
ing. Other sources of lead are presented in Table 11-60.
TABLE 11-60. SOURCES OF LEAD
Source
References
Colored Gift Wrapping
Gunshot Wound
Drinking Glass Decorations
Electric Kettles
Hair dye
Snuff use
Firing ranges
Gasoline Sniffing
Kaufman and Wiese (1978)
Coodin and Boeckx (1978)
Hansen and Sharp (1978)
Bertagnolli and Katz (1979)
Dillman et al. (1979)
Anonymous (1979)
Wigle and Charlebois (1978)
Searle and Harnden (1979)
Filippini and Simmler (1980)
Fischbein et al. (1979, 1980b)
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11.6 SUMMARY AND CONCLUSIONS
Studies of ancient populations using bone and teeth show that levels of internal exposure
of lead today are substantially elevated over past levels. Studies of current populations
living in remote areas far from urbanized cultures show blood lead levels in the range of 1 to
5 Mfl/dl. In contrast to the blood lead levels found in remote populations, data from current
U.S. populations have geometric means ranging from 10 to 20 ng/dl depending on age, race, sex
and degree of urbanization. These higher current exposure levels appear to be associated with
industrialization and widespread commercial use of lead, e.g. in gasoline combustion.
Age appears to be one of the single most important demographic covariates of blood lead
levels. Blood lead levels in children up to six years of age are generally higher than those
in non-occupationally exposed adults. Children aged two to three years tend to have the high-
est levels as shown in Figure 11-32. Blood lead levels in non-occupationally exposed adults
¦ay increase slightly with age due to skeletal lead accumulation.
Sex has a differential impact on blood lead levels depending on age. No significant dif-
ferences exist between males and females less than seven years of age. Males above the age of
seven generally have higher blood lead levels than females.
Race also plays a role, in that blacks generally have higher blood lead levels than
either whites or Hispanics and urban black children (aged 6 mo. to 5 yr.) have markedly higher
blood lead concentrations than any other racial or age group. Possible genetic factors asso-
ciated with race have yet to be fully disentangled from differential exposure levels as im-
portant determinants of blood lead levels.
Blood lead levels also generally increase with degree of urbanization. Data from NHANES
II show blood lead levels in the United States, averaged from 1976 to 1980, increasing from a
geometric mean of 11.9 pg/dl in rural populations to 12.8 pg/dl in urban populations less than
one million, increasing again to 14.0 pg/dl in urban populations of one million or more.
Recent U.S. blood lead levels show a downward trend occurring consistently across race,
age and geographic location. The downward pattern commenced in the early part of the 1970's
and has continued into 1980. The downward trend has occurred from a shift in the entire dis-
tribution and not through a truncation in the high blood lead levels. This consistency sug-
gests a general causative factor, and attempts have been made to identify the causative ele-
ment. Reduction in lead emitted from the combustion of leaded gasoline is a prime suspect, but
at present no causal relationship has been established.
Blood lead levels, examined on a population basis, have similarly skewed distributions.
Blood lead levels, from a population thought to be homogenous in terms of demographic and lead
exposure characteristics, approximately follow a lognormal distribution. The geometric stan-
dard deviations, an estimation of dispersion, for four different studies are shown in Table
11-61. The values, including analytic error, are about 1.4 for children and possibly somewhat
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40
30
28
20
1B
10
.*
IDAHO STUDY
NEW YORK SCREENING - BLACKS
NEW YORK SCREENING - WHITES
NEW YORK SCREENING - HISPANICS
NHANE8 II STUDY - BLACKS
NHANES II STUDY • WHITES
4 6 •
AGE IN YEARS
10
Figure 11-32. Geometric mean blood lead (avals by race and aga for younger children In the
NHANES II study, and the Kellogg/Silver Valley and New York Childhood Screening Studies.
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TABLE 11-61. SUMMARY OF POOLED GEOMETRIC STANDARD
DEVIATIONS AND ESTIMATED ANALYTIC ERRORS
Study
Pooled Geometric Standard Deviations
Estimated
Inner City
Black Children
Inner City
White Children
Adults
Females
Adult
Males
Analytic
Error
NHANES II
1.37
1.39
1.36a
1.40a
0.021
N.Y. Childhood
Screening Study
1.41
1.42
-
-
(b)
Tepper-Leven
-
-
1.30
-
O.Q56C
Azar et al.
-
-
-
1.29
0.042C
Note: To calculate an estimated person-to-person GSO, compute Exp [((In(GSD)) -
Analytic Error)*]
apooled across areas of differing urbanization
bnot known, assumed to be similar to NHANES II
ctaken from Lucas <1981).
smaller for adults. This allows an estimation of the upper tail of the blood lead distri-
bution, the group at higher risk.
Because the main purpose of this chapter is to examine relationships of lead in air and
lead in blood under ambient conditions, the results of studies most appropriate to this area
have been emphasized. A summary of the most appropriate studies appears in Table 11-62. At
3
air lead exposures of 3.2 pg/m or less, there is no statistically significant difference be-
tween curvilinear and linear blood lead inhalation relationships. At air lead exposures of 10
3
pg/m or more, either nonlinear or linear relationships can be fitted. Thus, a reasonably
consistent picture emerges in which the blood-lead air-lead relationship by direct inhalation
was approximately linear in the range of normal ambient exposures of 0.1 - 2.0 pg/m (as dis-
cussed in Chapter 7). Differences among individuals in a given study (and among several
studies) are large, so that pooled estimates of the blood lead inhalation slope depend upon
the the weight' given to various studies. Several studies were selected for analysis, based
upon factors described earlier, EPA analyses* of experimental and clinical studies (Griffin
et al. 1975; Rabinowitz et al., 1974, 1976, 1977; Kehoe 1961a,b,c; Gross 1981; Hammond et al.,
1981) suggest that blood lead in adults increases by 1.64 ± 0.22 pg/dl from direct Inhalation
"Note: The term EPA analyses refers to calculations done at EPA. A brief discussion of the
methods used is contained in Appendix 11-B; more detailed information is available at EPA upon
request.
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TABLE 11-62. SUMMARY OF BLOOD INHALATION SLOPES, (p)
pg/dl per pg/m
Population
Study
Study
Type
CP)
N Slope
fifl/dl per Mfl/m2
Model Sensitivity
Of Slope*
(1.40 - 4.M)1,2,3
(1.55 - 2.46)1,2
12 3
(1 07 - 1 52)
Children
Adult Males
Angle and
Mclntlre, 1979
Onaha, NE
Roels et al.
(1980)
Belgium
Yankel et al.
(1977); Walter
et al, (1980)
Idaho
Azar et al.
(1975). Five
groups
Griffin et al.
(1975), NY
pri soners
Gross
(1979)
Rabinowitz et
al. (1973,1976,
1977)
Population
Population
Population
Population
Experiment
Experiment
Experiment
1074
148
879
149
43
1.92
2.46
1.52
1.32
1.75
1.25
2.14
(1.08 - 2.39)
(1.52 - 3.38)4
(1.25 - 1.55)*
(2.14 - 3.51)S
2,3
*Selected from anoog the most plausible statistically equivalent models,
slope at 1.0 wo/a .
For nonlinear nodels,
Sensitive to choice of other correlated predictors such as dust and soil lead.
Sensitive to linear vs. nonlinear at low air lead.
3
Sensitive to age as a covariate.
i
Sensitive to baseline changes in controls.
^Sensitive to assumed air lead exposure.
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3
of each additional jig/m of air lead. EPA analyses of population studies (Yankel et al.,
1977; Roels et al., 1980; Angle and Mclntire, 1979) suggest that, for children, the blood lead
increase is 1.97 ± 0.39 Mfl/dl per ^or air lead. EPA anaylsis of Azar's population study
(Azar et al., 1975) yields a slope of 1.32 ± 0.38 for adult males.
These slope estimates are based on the assumption that an equilibrium level of blood lead
is achieved within a few months after exposure begins. This 1s only approximately true, since
lead stored in the skeleton may return to blood after some years. Chamberlain et al. (1978)
suggest that long term inhalation slopes should be about 30 percent larger than these
estimates. Inhalation slopes quoted here are associated with a half-life of blood lead in
adults of about 30 days. 0'Flaherty et al. {1982) suggest that the blood-lead half-life may
increase slightly with duration of exposure, but this has not been confirmed (Kang et al.,
1983).
One possible approach would be to regard all inhalation slope studies as equally infor-
mative and to calculate an average slope using reciprocal squared standard error estimates as
weights. This approach has been rejected for two reasons. First, the standard error estima-
tes characterise only the internal precision of an estimated slope, not its representativeness
(i.e., bias) or predictive validity. Secondly, experimental and clinical studies obtain more
information from a single individual than do population studies. Thus, it may not be appro-
priate to combine the two types of studies.
Estimates of the inhalation slope for children are only available from population
studies. The importance of dust ingestion as a non-inhalation pathway for children is estab-
lished by many studies. A slope estimate has been derived for air lead inhalation based on
those studies (Angle and Mclntire 1979; Roels et al., 1980; Yankel et al., 1977) from which
the air inhalation and dust ingestion contributions can both be estimated.
While direct inhalation of air lead Is stressed, this 1s not the only air lead contribu-
tion that needs to be considered. Smelter studies allow partial assessment of the air lead
contributions to soil, dust and finger lead. Conceptual models allow preliminary estimation
of the propagation of lead through the total food chain as shown in Chapter 7. Useful mathe-
matical models to quantify the propagation of lead through the food chain need to be
developed. The direct inhalation relationship does provide useful information on changes in
blood lead as responses to changes in air lead on a time scale of several months. The in-
direct pathways through dust and soil and through the food chain may thus delay the total
blood lead response to changes in air lead, perhaps by one or more years. The Italian HE
study facilitates partial assessment of this delayed response from leaded gasoline as a
source.
Dietary absorption of lead varies greatly from one person to another and depends on the
physical and chemical form of the carrier, on nutritional status, and on whether lead is
P811C/A 11-158 7/29/83
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PRELIMINARY DRAFT
ingested with food or between meals. These distinctions are particularly important for con-
sumption by children of leaded paint, dust and soil. Typical values of 10 percent absorption
of ingested lead into blood have been assumed for adults and 25 to 50 percent for children.
It is difficult to obtain accurate dose-response relationships between blood lead levels
and lead levels in food or water. Dietary intake must be estimated by duplicate diets or
fecal lead determinations. Water lead levels can be determined with some accuracy, but the
varying amounts of water consumed by different individuals adds to the uncertainty of the es-
timated relationships.
Quantitative analyses relating blood lead levels and dietary lead exposures have been re-
ported. Studies on infants provide estimates that are in close agreement. Only one indi-
vidual study is available for adults (Sherlock et al. 1982); another estimate from a number of
pooled studies is also available. These two estimates are in good agreement. Most of the
subjects in the Sherlock et al. (1982) and United Kingdom Central Directorate on Environmental
Pollution (1982) studies received quite high dietary lead levels (>300 jjg/day). The fitted
cube root equations give high slopes at lower dietary lead levels. On the other hand, the
linear slope of the United Kingdom Central Directorate on Environmental Pollution' (1982) study
is probably an underestimate of the slope at lower dietary lead levels. For these reasons,
the Ryu et al. (1983) study is the most believable, although it only applies to infants.
Estimates for adults should be taken from the experimental studies or calculated from assumed
absorption and half-life values. Most of the dietary intake supplements were so high that
3
many of the subjects had blood lead concentrations much in excess of 30-pg/m for a considera-
ble part of the experiment. Blood lead levels thus may not completely reflect lead exposure,
due to the previously noted nonlinearity of blood lead response at high exposures. The slope
estimates for adult dietary intake are about 0.02 (jg/dl increase in blood lead per pg/day in-
take, but consideration of blood lead kinetics may increase this value to about 0.04. Such
values are a bit lower than slopes of about 0.05 |jg/dl per pg/day estimated from the popula-
tion studies extrapolated to typical dietary intakes. The value for infants is larger.
The relation between blood lead and water lead is not clearly defined and is often de-
scribed as nonlinear. Water lead intake varies greatly from one person to another. It has
been assumed that children can absorb 25 to 50 percent of lead in water. Many authors chose
to fit cube root models to their data, although polynomial and logarithmic models were also
used. Unfortunately, the form of the model greatly influences the estimated contributions to
blood leads from relatively low water lead concentration.
Although there is close agreement in the quantitative analyses of the relationship bet-
ween blood lead level and dietary lead, there is a larger degree of variability in results of
the various water lead studies. The relationship is curvilinear, but its exact form 1s yet to
be determined. At typical levels for U.S. populations, the relationship appears linear. The
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PRELIMINARY DRAFT
only study that determines the relationship based on lower water lead values (<100 jig/1) is
the Pocock et al. (1983) study. The data from this study, as well as the authors theaselves,
suggest that in this lower range of water lead levels, the relationship is linear. Further-
more, the estiMated contributions to blood lead levels from this study are quite consistent
with the polynomial models from other studies. For these reasons, the Pocock et al. (1983)
slope of 0.06 is considered to represent the best estimate. The possibility still exists,
however, that the higher estimates of the other studies may be correct in certain situations,
especially at higher water lead levels {>100 jjg/1).
Studies relating soil lead to blood lead levels are difficult to compare. The relation-
ship obviously depends on depth of soil lead, age of the children, sampling method, cleanli-
ness of the home, mouthing activities of the children, and possibly many other factors. Var-
ious soil sampling methods and sampling depths have been used over time, and as such they may
not be directly comparable and may produce a dilution effect of the major lead concentration
contribution from dust which Is located primarily in the top 2 cm of the soil. Increases in
soil dust lead significantly increase blood lead in children. From several studies (Yankel et
al., 1977; Angle and Mclntire, 1979) EPA estimates an increase of 0.6 to 6.8 Mfl/dl in blood
lead for each Increase of 1000 pg/g in soil lead concentration. Values of about 2.0 jjg/dl per
1,000 yg/g soil lead from the Stark et al. (1982) study may represent a reasonable median
estimate. The relationship of housedust lead to blood lead 1s difficult to obtain. House-
hold dust also increases blood lead, children from the cleanest homes in the Silver Valley/
Kellogg Study having 6 jjg/dl less lead in blood, on average, than those from the households
with the most dust.
A number of specific environmental sources of airborne lead have been evaluated for pot-
ential direct influence on blood lead levels. Combustion of leaded gasoline appears to be the
largest contributor to airborne lead. Two studies used isotope ratios of lead to estimate the
relative proportion of lead in the blood coming from airborne lead. From one study, by
Wanton, it can be estimated that between 7 and 41 percent of the blood lead in study subjects
in Dallas resulted from airborne lead. Additionally, these data provide a means of estimating
the indirect contribution of air lead to blood lead. By one estimate, only 10 to 20 percent
of the total airborne contribution in Dallas is from direct inhalation.
From the ILE data in Facchetti and Geiss (1982), as shown in Table 11-63, the direct in-
halation of air lead may account for 5* percent of the total adult blood lead uptake from
leaded gasoline In a large urban center, but inhalation 1s a much less important pathway in
suburban parts of the region (17 percent of the total gasoline lead contribution) and in the
rural parts of the region (8 percent of the total gasoline lead contribution). EPA analyses
of the preliminary results from the ILE study separated the inhalation and non-inhalation con-
tributions of leaded gasoline to blood lead into the following three parts: (1) An increase
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PRELIMINARY DRAFT
3
of about 1.7 pg/dl In blood lead per |jg/m of air lead, attributable to direct inhalation of
the combustion products of leaded gasoline; (2) a sex difference of about 2 pg/dl attributable
to lower exposure of women to indirect (noninhalation) pathways for gasoline lead; and (3) a
non-inhalation background attributable to indirect gasoline lead pathways, such as ingestion
of dust and food, increasing from about 2 yg/dl in Turin to 3 Mfl/dl in remote rural areas.
The non-inhalation background represents only two to three years of environmental accumulation
at the new experimental lead isotope ratio. It is not clear how to extrapolate numerically
these estimates to U.S. subpopulations; but it is evident that even in rural and suburban
parts of a metropolitan area, the indirect (non-inhalation) pathways for exposure to leaded
gasoline make a significant contribution to blood lead. This can be seen in Table 11-63. It
should also be noted that the blood lead isotope ratio responded fairly rapidly when the lead
isotope ratio returned to its pre-experimental value, but it is not yet possible to estimate
the long term change in blood lead attributable to persistent exposures to accumulated envi-
ronmental lead.
Studies of data from blood lead screening programs suggest that the downward trend In
blood lead levels noted earlier is due to the reduction in air lead levels, which has been at-
tributed to the reduction of lead in gasoline.
TABLE 11-63. ESTIMATED CONTRIBUTION OF LEADED GASOLINE TO BLOOD LEAD
BY INHALATION AND NON-INHALATION PATHWAYS
Air Lead
Fraction
From
Gasoline
(a)
Blood
Lead
Fraction
From
Gasoline
(b)
Blood Pb
From
Gasolipex
In Air
Blood Lead
Not Inhaled
Fr»(8,S.-
Estimate
Fraction
Gas-Lead
Inhalation
(e)
Location
Mg/dl
pg/dl
Turin 0.873 0.237 2.79 2.37 0.54
<25 km 0.587 0.125 0.53 2.60 0.17
>25 km 0.587 0.110 0.28 3.22 0:08
(a) Fraction of air lead 1n Phase 2 attributable to lead in gasoline.
(b) Mean fraction of blood lead in Phase 2 attributable to lead in gasoline.
(c) Estimated blood lead from gas inhalation = p x (a) x (b), p = 1.6.
(d) Estimated blood lead from gas, non-Inhalation = (f)-(e)
(e) Fraction of blood lead uptake from gasoline attributable to direct Inhalation = (f)/(e)
Source: Facchettl and Geiss (1982), pp. 52-56.
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Primary lead smelters, secondary lead smelters and battery plants earit lead directly into
the air and ultimately increase soil and dust lead concentrations in their vicinity. Adults,
and especially children, have been shown to exhibit elevated blood lead levels when living
close to these sources. Blood lead levels in these residents have been shown to be related to
air, as well as to soil or dust exposures.
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I11REF/A
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APPENDIX 11A
COMPARTMENTAL ANALYSIS
Many authors have noted that under conditions of constant lead exposure, blood lead con-
centrations change from one level to another apparent equilibrium level over a period of
several months. A mathematical model is helpful in estimating the new apparent equilibrium
level even when the duration of the experiment is not sufficiently long for this equilibrium
level to have been achieved. The model assumes that lead in the body is held in some number
of homogeneous and well-mixed pools or compartments. The compartments have similar kinetic
properties and may or may not correspond to identifiable organ systems. In a linear kinetic
model it is assumed that the rate of change of the mass of lead in compartment 1 at time t,
denoted X^(t), is a linear function of the mass of lead in each compartment. Denote the frac-
tional rate of transfer of lead into compartment i from compartment j by K.j (fraction per
day), and let I.(t) be the total external lead input Into compartment i at time t in units
such as pg/day. The elimination rate from compartment i is denoted K^. The conpartnental
model is:
dX.(t)/dt = I.(t) + Kn XjU)* * • • + KinXn(t) - (Kq. + Kxi + • 1 * + Kni)X.(t)
for each of the n compartments. If the inputs are all constant, then each X^(t) is the sum of
(at most) n exponential functions of time (see for example, Jacquez, 1972).
For the one-compartment model:
dXj(t)/dt - Ix - K01 X^t)
with an initial lead burden Xj(0) at time 0,
XjCt) = XjCO) exp(-K01t) + [ (l-exp(-K01t)]
The mass of lead at equilibrium is M9- w® may think of this pool as "blood lead". If
the pool has volume then the equilibrium concentration is jjg/dl. Intake from
several pathways will have the form:
Ix = A2 (Pb-Air) ~ A2 (Pb-Diet)+ ' ' *
so that the long term concentration is
V*01 V1"
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PRELIMINARY DRAFT
The Inhalation coefficient is p = *l^K01Vl* The b1oocl lead half-life is 0.693/Kq^.
Models with two or more compartments will still have equilibrium concentrations in blood
and other compartments that are proportional to the total lead intake, and thus increase
linearly with Increasing concentrations in air, dust, and diet. The relationship between the
exponential parameters and the fractional transfer coefficients will be much more complicated,
however.
Models with two or three pools have been fitted by Rabinowitz et al. (1976, 1977) and by
Batschelet et al. (1979). The pools are tentatively identified as mainly blood, soft tissue
and bone. But as noted in Section 11.4.1.1, the "blood" pool is much larger than the volume
of blood itself, and so it is convenient to think of this as the effective volume of distri-
bution for pool 1. A five-pool model has been proposed by Bernard (1977), whose pools are
mainly blood, liver, kidney, soft bones and hard bone.
The major conclusion of this Appendix is that linear kinetic mechanisms imply linear
relationships between blood lead and lead concentrations in environmental media. Any extended
discussion of nonlinear kinetic mechanisms is premature at this point, but it Is of some
interest that even simple nonlinear kinetic models produce plausible nonlinear blood lead vs.
concentration relationships. For example, if the rate of blood lead excretion into urine or
storage "permanently" in bone increases linearly with blood lead, then at high blood lead
levels, blood increases only as the square root of lead intake. Let M denote the mass of lead
in pool 1 at which excretion rate doubles. Then:
dXj(t)/dt = I2 - K01(l ~ X1(t)/M1)X1(t)
has an equilibrium level:
Xx = M1(V 1 + 4I1/KQ1M1 - 1)/2
This is approximately linear in intake I when 1^ 1s small, but a square root function of In-
take when it is large. Other plausible models can be constructed.
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APPENDIX 116
FITTING CURVES TO BLOOD LEAD DATA
The relationship between blood lead and the concentrations of lead in various environ-
mental media is a principal concern of this chapter. It is generally accepted that the geo-
metric mean blood lead is some function, f, of the concentration of air lead and of lead in
diet, dust, soil and other media. It has been observed that blood lead levels have a highly
skewed distribution even for populations with relatively homogeneous exposure, and that the
variability in blood lead is roughly proportional to the geometric mean blood lead or to the
arithmetic mean (constant coefficient of variation). Thus, instead of the usual model in
which random variations are normally distributed, a model is assumed here in which the random
deviations are multiplicative and lognormally distributed with geometric mean 1 and geometric
standard deviation (GSD) e°. The model is written
Pb-Blood = f (Pb-Air, etc.) eoz
where z is a random variable with mean 0 and standard deviation 1. It has a Gaussian or
normal distribution. The model is fitted to data in logarithmic form
In(Pb-Blood) = In (f)
even when f is assumed to be a linear function, e.g.,
f = p Pb-Air 4 PQ + Pj Pb-Dust + ...
The nonlinear function, fitted by most authors (e.g., Snee, 1982b), is a power function with
shape parameter A,
f = (p Pb-Air + pQ + Pb-Dust + ,..)k
t
These functions can all be fitted to data using nonlinear regression techniques. Even when
the nonlinear shape parameter A has a small statistical uncertainty or standard error as-
sociated with it, a highly variable data set may not clearly distinguish the linear function
(X = 1) from a nonlinear function (X ^ 1). In particular, for the Azar data set, the residual
sum of squares is shown as a function of the shape parameter A, in Figure 11B-1. When only a
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9.3
8,7
8.6
"I I I I
1 1 1 1
—
MINIMUM SIGNIFICANT
DIFFERENCE FOR 1 DF
—
— 1 6
SSE FOR In (Pb-Btood) - A In (j? Pb-Air+I^
CJ) -
L 1=0.26
—
MINIMUM SIGNIFICANT
DIFFERENCE FOR B DF
—
—
6 6
^SSE FOR In IPb-Blood)=A In (0 Pb-Alr+I/J. C.+I/J', C. Aa«l —
1 J J 1 i )
1-1
I ~
—
III!
1 1 1 1
0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0
POWER EXPONENT, A
Figure 11 B-1. Residual sum of squares for nonlinear regression models for Azar
data
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PRELIMINARY DRAFT
separate intercept (background) is assumed for each subpopulation, the best choice is k =
0 26; but when age is also used as a covariate for each subpopulation, then the linear model
is better. However, the approximate size of the difference, in residual sum of squares
required to decide at the 5 percent significance level that a nonlinear model is better (or
worse) than a linear model, is larger than the observed difference in sum of squares for any
A>0.2 (Gallant, 1975). Therefore a linear model is used unless evidence of nonlinearity is
very strong, as with some of Kehoe's studies and the Silver Valley/Kellogg study. Non-
linearity is detectable only when blood lead is high (much above 35 or 40 >jg/dl), and intake
is high, e.g., air lead much above 10 (jg/m^.. Additional research is needed on the relation-
ship between lead levels and lead intake from all environmental pathways.
The "background" or intercept term pg in most models requires some comment. As the
Manton and Italian lead isotope studies show, lead added to a regional environment by combus-
tion of gasoline accumulates a large non-inhalation component even after only 2 years (see
Figure 11-26). The non-inhalation contribution in the Turin region was nearly independent of
location (air lead). It is not possible to assign causes, e.g., ingestion of food, dust, or
water by adults, so no direct extrapolation to U.S. populations is possible at this time due
to unknown differences in non-air exposures between the U.S. and Italy. It is probable that
the non-inhalation contribution to blood lead increases with time as lead accumulates in the
environment. After many years, one might obtain a figure like Figure 118-2. Another concept
is that such a curve should predict zero blood lead increase at zero air lead. If the blood
lead curve is forced to pass through 0 when air lead = 0, a nonlinear curve is required. It
has been concluded that a positive intercept term is needed to account for intake from
accumulated lead in the environment, which precludes fully logarithmic models such as
In (Pb-Blood) = In (pQ) + p In (Pb-Air) + In (Pb-Dust) + ...
It must be acknowledged that such models may provide useful interpolations over a range of air
lead levels; e.g., the Goldsmith-Hexter equation predicts blood lead 3.4 pg/dl at an air lead
<0.004 pg/m3 in the Nepalese subjects in Pioinelli et at. (1980).
The final concern is that the intercept term may represent indirect sources of lead expo-
sure that include previous air lead exposures. To the extent that present and previous air
lead exposures are correlated, the intercept or background term may introduce apparent curvi-
linearities in the population studies of inhalation. The magnitude of this effect is unknown.
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V
TOTAL CONTRIBUTION OF AIR LEAD AFTER
LONG INTERVAL OF EXPOSURE AND DEPOSITION
NON-INHALATION
BACKGROUND
CONCENTRATION
AFTER LONG
INTERVAL
OF AIR LEAD
EXPOSURE AND
DEPOSITION ^
V.
TOTAL CONTRIBUTION OF AIR
LEAD AFTER SHORT INTERVAL
OF EXPOSURE AND DEPOSITION
U-"
NON-INHALATION
BACKGROUND
CONCENTRATION
AFTER SHORT
INTERVAL OF
AIR LEAD
EXP08URE AND ,
DEPOSITION.
DIRECT INHALATION
OF AIR LEAD FROM
CURRENT EXPOSURE
I.
AIR LEAD CONCENTRATION
Figure 11 B-2. Hypothetical relationship between blood lead and air lead by
Inhalation and non-Inhalation.
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PRELIMINARY DRAFT
APPENDIX 11C
ESTIMATION OF GASOLINE LEAD CONTRIBUTIONS TO ADULT
BLOOD LEAO BURDENS BASED ON ILE STUDY RESULTS
As discussed in Chapter 11 (pp. 11-118 to 11-123) the results of the Isotopic Lead Ex-
periment (ILE) carried out in Northern Italy provide one basis by which to estimate contribu-
tions of lead in gasoline to blood lead burdens of populations exposed in the ILE study area.
Figures 1 to 5 of this appendix, reprinted from the ILE Status Report (1982) illustrate
changes in isotopic lead (206/207) ratios for 35 adult subjects, for whom repeated measure-
ments were obtained over time during the ILE study. The percent of total blood lead in those
subjects contributed by Australian lead-labelled gasoline (petrol) used in automotive vehicles
in the ILE study area was estimated by the approach reprinted below verbatim from Appendix 17
of the ILE Status Report (1982):
The main purpose of the ILE project was the determination of the contribution of petrol
lead to total lead in blood. A rough value for the fraction of petrol lead in blood can be
derived from the following equations:
each of them referring to a given time at which equilibrium conditions hold.
R' and R" represent the blood lead Isotopic ratios measured at each of the two times; if
Rj and R£ represent the local petrol lead isotopic ratios measured at the same times, X is the
fraction of local petrol lead in blood due to petrols affected by the change in the lead iso-
topic ratio, irrespective of its pathway to the blood i.e. by inhalation and ingestion (e.g.
from petrol lead fallout). The term (1-X) represents the fraction of the sum of all other
external sources of lead in the blood (any «other» petrol lead included), factor f being the
unknown isotopic ratio of the mixture of these sources. It is assumed that X and f remained
constant over the period of the experiment, which implies a reasonable constancy of both the
lead contributing sources in the test areas and the living habits which, in practice, might
not be entirely the case.
Data from individuals sampled at the initial and final equilibrium phases of the ILE
study together with petrol lead isotopic ratios measured at the sane times, would Ideally pro-
vide a means to estimate X for Turin and countryside adults. However, for practical reasons,
calculations were based on the initial and final data of the subjects whose first sampling was
Rx X + f (1-X) = R'
R2 X + f (1-X) = R"
(1)
(11)
DUP11/B
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PRELIMINARY" DRAFT
done not later than 1975 and the final one during phase 2. Their complete follow-up data are
shown in Table 27. For and R,, the values measured in the phases 0 and 2 of ILE were used
(R^ = 1.186, R2 = 1.060). Hence, as averages of the individual X and f results, we obtain:
Turin X, = 0.237 ± 0.054 i.e 24%
f£ = 1.1560 ± 0.0033
countryside X, = 0.125 ± 0.071 i.e. 12%
<25 km f| = 1.1542 ± 0.0036
countryside * X- = 0.110 ± 0.058 i.e 11%
>25 Ion f| = 1.1576 ± 0.0019
Fig. 1. Individual valuet of blood Pb-206/Pb-207 ratio for subject! follow-up in Turin (12 nibjects)
DUP11/B
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Piatt 2
Fi|. 2. Individual vtluei in blood Pb-206/Pb-207 ratio for subjects follow-up in Gutagneto (4 subjects)
WOi/FW
W-
IS-
IM-
113-
112-
¦o— MUUTO
FIANO
PkitiO
Plttnl
HnstS
DUP11/B
M I 75 I 78 1 ?7 ' 71 I 71 I *
Fig. 3, Individual vriues of Mood Pb-2Q6/Pb-207 ratio fof wbjecti follow-up in Drum to and Futoo (6 »ub]oct»)
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PRELIMINARY DRAFT
P»2K/PM07
lt»-
IB-
m-
lt3"
—•— SANTEM
—o— MR.E
IB-
PkniO
"T
74
Pkmt
Pkw2
T
76
77 1 7« I 79 1 10
Fig. 4. Individual value* of Mood Pb-206/Pb-207 ratio for mtyecti follow-up in Nole and Swwt (9 wbjecti)
75 I 71 T 77 I 7| I 79 I II
Fig. 5. Individual valuta of Mood Pb-206/Ft>-207 ratio for ntyacts follow-up in Viii (4 autyecta)
DUP11/B
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APPENDIX 11-D
REPORT
OF THE
NHANES II TIME TREND ANALYSIS REVIEW GROUP
June 15, 1983
SRD/NHANES
(11D-1)
6/22/83
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
Environment*) Criteria and Assessment Office (MD-52)
Research Triangle Perk, North Carolina 27711
The materials contained in this report were generated as the result of critical
evaluations and deliberations by members {listed below) of the NHANES II Time Trend
Analysis Review Group. All members of this Review Group unanimously concur with
and endorse the findings and recommendations contained in the present report as
representing the collective sense of the Review Group.
Dr. Joan Rosenblatt (Chairman)
Deputy Director
Center for Applied Mathematics
National Bureau of Standards
Washington, D. C. 20234
Dr. Harry Smith, Professor
Chairman, Department of
Biomathematical Science
Mt. Sinai School of Medicine
New York, New York 10029
Dr. Richard Royal 1, Professor
Department of Biostatistics
Johns Hopkins University
615 North Wolfe Street
Baltimore, Maryland 21205
Dr. J, Richard landis, Professor
Department of Biostatistics
School of Public Health II
University of Michigan
Ann Arbor, Michigan 18109
Dr. Roderick Little
American Statical Assoc. Fellow
Bureau of Census
Department of Commerce
Washington, D. C.
(11D-2)
-------
Table of Contents
Summary i 1
Introduction 1
Time Trends in Blood-Lead Values 2
Measurement Quality Control 2
Nonresponse 3
Survey Design 3
Sample Weights 5
Estimated Time Trends 6
Summary 6
Correlation Between Blood-Lead and Gasoline-Lead Levels 7
Preliminary Remarks 7
Variables Used in the Analyses 8
Statistical Techniques Used in the Analyses 11
Models Used in the Analyses 11
Gasoline Lead as a Causal Agent for the Decline
in Blood-Lead Levels 12
Use of NHANES II Data for Forecasting Results of
Alternative Regulatory Policies ~ 13
Summary 13
References 14
Appendix 01 - Questions for the Review Group 15
Appendix D2 - Documents Considered by the Review Group 16
Appendix D3 - List of Attendees at Review Group Meetings 19
(111^-3)
-------
Summary
The Review Group finds strong evidence that there was a substantial decline in
the average level of blood lead in the U.S. population during the NHANES II
survey period. After adjustment for relevant demographic covariat-les, the
magnitude of the change can be estimated for the total U.S. population and for
some major subgroups, provided careful attention is given to underlying model
assumptions.
The Review Group also finds a strong correlation between gasoline-lead usage
and blood-lead levels. In the absence of scientifically plausible alternative
explanations, the hypothesis that gasoline lead is an Important causal factor
for blood-lead levels must receive serious consideration. Nevertheless,
despite the strong association between the decline in gasoline-lead usage and
the decline in blood-lead levels, the survey results and statistical analyses
do not confirm the causal hypothesis. Rather, this finding is based on the
qualitatively consistent results of extensive analyses done in different but
complementary ways.
The gasoline lead coefficient in regressions of blood-lead levels on that
variable, adjusted for observed covariates, has been used to quantify the
causal effect of gasoline lead on blood-lead levels. The Review Group
considers that such inferences require strong assumptions about the absence of
effects from other unmeasured lead sources, the adequacy of national gasoline
lead usage as a proxy for local exposure, and the adequacy of a sample design
which does not measure changes in blood-lead levels for individuals in the
sample. The validity of these assumptions could not be determined frorn the
NHANES II data or from other data supplied to the Review Group. Furthermore,
the Review Group cautions against extrapolation of the observed relationship
beyond the limits of the four year period.
, i 1 .
(110-4)
-------
Introduction
This Review Group was appointed in February, 1983 by the Director of the
Environmental Criteria and Assessment Office, U.S. Environmental Protection
Agency (EPA), to consider a series of questions about the interpretation of
data from the second National Health and Nutrition Examination Survey (NHANES
II) to evaluate relationships over time between blood-lead levels and gasoline
lead usage. The questions addressed to the Review Group are listed in full in
Appendix 01.
Documents describing NHANES II, analyses of the survey data, and analyses of
the relationships between blood-lead values and gasoline lead usage were
furnished for review. In two meetings, on March 10-11 and March 30-31, 1983,
the Review Group discussed these materials with officials of the EPA, and with
specialists from the several institutions that had conducted these studies.
The documents provided for review are listed in Appendix D2. The individuals
who attended the two meetings are listed in Appendix 03.
The panel members of the Review Group are statisticians with experience in
applications of statistics in the physical, biomedical, and social sciences,
but had no previous involvement in analyses of data about blood lead or
gasoline lead. The affiliations of the panel members are listed in Appendix
03 for identification; views expressed by the panel in this report are their
own and not those of the institutions.
Agencies involved in the conduct of the NHANES II were the National Center for
Health Statistics (NCHS), the Centers for Disease Control (CDC) where the
chemical analyses were done, and the Food and Drug Administration (FDA).
Contributors to the analysis of the association between blood lead and
, gasoline lead usage, in addition to NCHS and C0C, are E. I. OuPont de Nemours
& Co. (DuPont), The Ethyl Corporation (Ethyl), and the EPA Office of Policy
Analysis working in collaboration with ICF Incorporated (ICF) and Energy and
Resource Consultants, Inc. (ERC).
This report contains two major sections. The first, on time trends in
blood-lead levels, addresses a set of questions about the use of NHANES II
data to estimate changes over time. The second addresses statistical aspects
of evaluating the relationship of changes in blood-lead levels to gasoline
lead usage.
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Time Trends In Blood-lead Values
At its first meeting on March 10-11, 1983, the Review Group considered only
the first of the set of questions presented to it (see Appendix 01), namely
questions about the extent to which the NHANES II data could be used to
"determine time trends for changes 1n nationally representative blood-lead
values for the years of the study (1976-1980)."
The phrases "define tine trends" and "determine time trends ... (1976-1980)"
are interpreted throughout this report to mean "estimate changes in blood-lead
values during the survey period," In particular, such changes are not to be
interpreted as trends that might be extrapolated.
The Group recognized that the survey was designed as a cross-sectional survey,
and specifically inquired into three general kinds of possible sources of
time-related bias:
- the measurement quality control,
- the nonresponse experience, and
- the survey design.
As would be expected, only incomplete evidence could be made available in each
of these areas. The following assessment of this evidence indicates where it
depends on the expert opinion of others.
Measurement Quality Control
In order to analyze the time trends in NHANES II data, one must assume that
the procedures for collecting, handling, and analyzing blood specimens did not
change during the survey years. The Review Group is aware that contamination
can produce spuriously high values in determination of trace elements, and
sought evidence that quality control procedures were equally stringent at all
times.
Although no quality control specimens were prepared at the medical examination
sites, the Review Group has been assured that training, periodic retraining,
materials, equipment, and procedures were designed to prevent contamination,
and not changed. There was some turnover of personnel.
The COC laboratory established and documented the results of extensive quality
control sampling (App. 02, item 14). The data on lead levels in the "blind"
samples, from two pools of bovine blood, exhibit essentially constant means
and standard deviations. The coefficient of variation for measurement error
was found to be about 17 percent for blood-lead levels near 13 pg/dL; it was
smaller, about 13 percent, for higher blood-lead levels near 25 pg/dl.
Additional evidence of the constancy of quality control is that data from
other analyses of the blood specimens (zinc, for example) exhibit little or no
change over time.
The Review Group finds no evidence that field and laboratory quality control
changes could account for the observed change in blood-lead levels.
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Nonresponse
Nonresponse is an important potential source of bias in sample surveys. It is
of particular concern in the blood-lead analysis of the NHANES II since the
nonresponse rate is high—39.3 percent of sampled persons had missing lead
values due to nonresponse at various stages of participation in the survey
(App. 02, item 14, p.9). The NCHS attempted to adjust for nonresponse by
(freighting responding individuals by estimates of the probability of response,
calculated within subclasses of the population formed by joint levels of age,
income, SMSA/non-SMSA, and region.
This is a standard adjustment method for unit nonresponse in surveys. The
method adjusts for differential nonresponse across the subclasses used to
calculate the weight, but does not account for residual association between
nonresponse and time and blood-lead level, which are the variables of primary
interest in the analysis under consideration. Thus there is the possibility
that nonresponse bias is a contributory factor to the trend in blood-lead
levels across time.
In order for nonresponse to have this effect it is necessary that, after
adjusting for the socioeconomic variables used to define the weights,
nonresponse be related to blood-lead level, and further that this relationship
change over time, so that a differential bias in the mean blood-levels of
respondents exists across time. Clearly this question cannot be addressed
directly, since the blood-lead levels of nonrespondents are not measured.
However, the Review Group considered such an interaction to be highly
unlikely, for the following reasons:
0 Nonresponse rates did not vary in a consistent way across
time. Examination of changes in response rates does not
indicate any relationship of importance (App. D2, item 18).
0 There does not appear to be evidence that the conditions of
the survey changed significantly across time, so that any bias
introduced by art association between nonresponse and
blood-lead level is unlikely to change across time.
Accordingly, the Review Group rejected nonresponse as a likely explanation for
the trend observed in the data.
Survey Design
The NHANES II was designed to provide U.S. national prevalence rates for a
wide range of characteristics and health conditions. Due to financial and
logistical constraints, the survey design required a four-year data collection
period. Consequently, the sample quantities, such as the blood-lead levels,
necessarily will provide period prevalence estimators, rather than point
prevalence estimators of the underlying population parameters. In general
practice, a fundamental assumption underlying the use of period data to
generate prevalence estimators is that the condition under investigation
remains relatively constant throughout the survey period.
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Even though the NHANES II was not designed to detect arid estimate changes in
prevalence throughout the survey period, one must consider the possibility
that the level of a particular target characteristic, such as blood lead,
actually may be changing over time. Consequently, one cannot ignore evidence
suggesting that the level of lead in blood in the U.S. population was
decreasing during the data collection period simply because the survey design
was cross-sectional, rather than longitudinal. Rather, the difficult question
is to what extent, if any, can these NHANES II data be used to determine time
trends.
Although a cross-sectional design such as the one utilized in the NHANES II
certainly is not optimal for investigating time trends, one can consider
making adjustments within the sample for the effects of relevant covariables
such as age, sex, race, residence, and income, if the distributions of these
covariables are not highly confounded with time. An additional requirement
for making adjustments is that there be reasonably large numbers of sample
persons for different covariable levels at various times. These internal
adjustments permit one to examine whether the decline in blood-lead levels can
be accounted for by differing proportions of individuals from subgroups
determined by relevant covariables. The extent of this type of selection bias
over time relative to primary demographic characteristics can be summarized
(App. D2, item 20, Tables M7, M8 for whites, and M13, M14 for blacks).
The Review Group considered carefully the potential bias due to changing
composition of the sample over time, especially since this had been emphasized
by Ethyl (App. D2, items 25, 26). The most striking problem occurs with urban
vs. rural groups. The fractions of blood samples obtained from white urban
residents are shown as follows:
Thus, there has been a striking decrease in the number of bloods taken from
white urbanites across the four years. If one assumes that exposure to lead
from gasoline is more prevalent in urban areas, then (without adjustment) the
observed mean blood levels across the four years would be biased because of
the NHANES II schedule.
Further examination of the CDC tabulation (App. D2, item 20) indicates sparse
information on blacks. The numbers are so small that time trend Inferences
for blacks can be estimated with confidence only for overall mean blood-lead
level results without regard to sex, place of residence, and age.
% urban bloods Sample size
Jan - Jun 1976
Jul - Dec 1976
Jan - Jun 1977
Jul - Dec 1977
Jan - Jun 1978
Jul - Dec 1978
Jan - Jun 1979
Jul - Dec 1979
Jan 1980
64.2
36.9
44.6
57.3
46.3
40.6
31.6
20.7
0.0
795
1255
935
1010
1056
981
1228
842
267
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The Review Group finds that despite obvious trends over time for such
characteristics as degree of urbanization and the proportion of children aged
0.5 to 5 years, the sample size is distributed across the grid of covariable
levels sufficiently to permit reasonable adjustments. In support of this
finding, the Review Group notes that similar trends appeared whenever
demographic subgroups were examined separately. These subgroups included
white males, white females, white children, white teenagers, white adults, and
blacks, as well as breakdowns by income and urban-rural status.
Sample Weights
Another possibility is that the sample mean blood-lead level changes resulted
from trends in more subtle statistical characteristics of the sample over
time, such as characteristics related to the way sample weights are used to
calculate averages. But thi« explanation appears to be inconsistent with the
fact that analyses of the unweighted NHANES II data lead to essentially the
same results as the weighted data and analysis.
In response to questions raised by both industry representatives and other
observers, the Review Group explored the effects of the complex weighting
scheme inherent in all the CDC and EPA/ICF analyses. Each sample observation
has both a basic weight (related to the probability of selection), a final
weight (reflecting additional adjustments to the basic weight accounting for
nonresponse patterns of selected demographic subgroups), and a final examined
lead subsample weight (corresponding to the entire set of adjustments due to
the probability of selection, nonresponse, and post-stratification, and the
subsampling of individuals selected for the measurement of blood lead). All
the weighted analyses in the CDC and EPA/ICF reports were conducted relative
to the final examined lead subsample weight.
One potential problem associated with this final lead subsample weight is the
possibility that differential nonresponse patterns for various demographic
subgroups may lead to marked differences between the basic weight (without
nonresponse adjustments) and this final weight. For that reason, the Review
Group requested a data display of the total nonresponse rate and the average
blood-lead levels by the 64 separate stands using three different weighting
schemes in computing the averages:
i) unweighted;
ii) basic weights;
iii) final lead subsampling weights.
As shown in Table 1, item 18 of App. D2, the average blood-lead levels are
quite consistent under each weighting scheme for each of the 64 stands.
Furthermore, there is no apparent trend in the nonresponse rate across time.
Consequently, one would expect that an analysis of these data under the basic
weights also would parallel the results obtained in the CDC and the ICF
reports.
These findings, in conjunction with the similarities between the weighted and
unweighted analyses, lend additional support to the overall consensus among
panel members that these data analyses are not dependent on the particular
choice of weights, including the intermediate basic weights.
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Estimated Time Trends
There seems to be no doubt that, qualitatively, a downward trend of blood-lead
levels has been observed during the NHANES II survey.
The data appear to support reasonably precise estimates of the magnitude of
t!.t change for a few major subgroups of the population. In particular, the
change in mean blood-lead levels during the survey period can be estimated for
the population as a whole and for population sectors grouped by age, sex,
race, urban/rural, and income, if each of these demographic categories is
considered separately.
For estimating changes in mean blood-lead levels for combinations of
demographic factors, sufficient data appeared to be available for white-by-sex
and white-by-age breakdowns. These estimated changes, and others that might
be considered, can be made on the basis of a linear model that provides
adjustments for demographic and socioeconomic covariables that are known or
believed to be associated with blood-lead levels.
For finer subdivisions, estimates of change are subject to large sampling
error and are sensitive to correct specification of the regression model.
Hence, caution must be exercised in their interpretation. It is not possible
to show time changes in mean blood levels for specific cities, towns, or
locales using the NHANES II data, since no city or locale was sampled more
than once. No data which would allow estimates of time trends in mean
Mood-lead levels for different occupational categories were shown to the
Review Group. The only socioeconomic variable considered was income.
Estimates of change, e.g., those reported by CDC (App. 02, item 14, Table 6,
page 44), should be accompanied by standard errors. There should be
discussions of the use of regression diagnostics to evaluate the adequacy of
the model, and the possibility that a few observations exert an excessive
influence on the result. The calculation of standard errors should use
procedures that take into account the stratification and clustering properties
of the survy design. In response to the Review Group's questions, CDC
provided a document presenting standard errors and the methodology used to
estimate them (App. 02, item 38). The size of these standard errors suggests
that there are only weak indications of differences between subgroups with
respect to the percent drop in the average blood-lead level.
Summary
Although the survey was not specifically designed to measure trends, data from
the NHANES II can be used to estimate changes in blood-lead levels during the
four-year period, 1976-1980, of the survey. Changes can be estimated for the
U.S. population and for major population subgroups, as specified in the
previous subsection. Because of sampling error, laboratory measurement error,
a high nonresponse rate, and the need to adjust for time-related imbalance in
the survey design, such estimated changes should be interpreted with caution.
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Correlation Between Blood-Lead and Gasoline-Lead Changes
At its second meeting on March 30-31, 1983, the Review Group considered three
sets of studies that examine the association between changes in blood-lead
levels estimated from the NHANES II data and changes in the use of leaded
gasoline:
- the Ethyl Corp. analysis (App, D2, items 25, 26)
- the ICF/EPA analysis (App. 02, items 11, 22, 23, 24), and
- the CDC/NCHS analysis (App. 02, item 14 and appendices).
The following discussions summarize the Review Group's assessment of the
strengths and weaknesses of the analyses.
Preliminary Remarks
The analyses propose and evaluate models for the relationship between
blood-lead levels and gasoline-lead usage. All of these analyses rely on
multiple linear regression methods, whose limitations with respect to
establishing causal relations are well known (See, e.g., reference 1). The
statistician-reviewer may adopt one or the other of two approaches in
considering the strengths and weaknesses of the several analyses:
(1) Assume (on external authority) the existence of a causal
relationship between gasoline lead usage and blood lead levels. Consider the
variables and models used to analyze the strength of the association and to
estimate the effect of gasoline-lead changes on blood-lead changes. In this
approach, the possible effects of other changes over time that affect
blood-lead levels are treated as second-order effects. CDC urges this
approach.
(2) Adopt a neutral position as to the causal relationships, and examine
the associations among the variables studied. In this approach, "time" serves
as a proxy for the combined effect of whatever changes affected blood-lead
levels and it is left to the interpreter of the analyses to assign relative
importance among suggested explanations for changes over time. DuPont and
Ethyl suggest this approach.
The ICF and CDC analyses both found a clear relationship between gasoline lead
and blood lead. The Ethyl analysis found no evidence of association between
these variables. The purpose of this commentary is to discuss the important
differences between the analyses and to assess their utility in establishing
or contradicting the hypothesized relationship between the decline in
blood-lead levels and the decline in gasoline lead emissions over the period
of the NHANES II Survey.
Table I (next page) classifies the three analyses by six factors which capture
the main differences between them, namely: 1) the choice of measure of
gasoline lead, 2) the scale of blood lead variable, raw or logarithm, 3) the
unit of analysis, 4) control variables in the regression, and in particular
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the inclusion or omission of a time variable, 5) the weighting used in the
regressions, and 6) the method used to calculate standard errors. The panel
concludes that of these factors only (1) and (4) had a substantial impact on
the final results.
Table 1
1) measure of gasoline
lead
2) scale of dependent
variable
3) unit of analysis
4) control variables
include time
5) weighting by
selection probs.
6) design based
standard errors
CDC
quarterly
log
individual
no
both
yes
ICF
monthly sales
x lead conc.
raw
individual
time, season,
lagged gas
yes -
yes
Ethyl
pop. density
local lead usage
raw
individual stage 1
locality stage 2
time
no
no
The first three factors are discussed under the heading "Variables Used in the
Analyses". Factors (4), (5), and (6) are discussed under "Statistical
Techniques Used in the Analyses". Factor (4) is considered further in the
assessment of "Models Used in the Analyses".
Variables Used in the Analyses
Demographic and socioeconomic covariables were used as defined for the NHANES
II Survey. Differences between the analyses occurred 1n the choice of
specific representations for blood-lead levels and gasoline lead usage.
Blood Lead. All the studies used blood-lead values for individuals from the
MhANES II Public Use Data Tape, with associated demographic, economic, time,
and sampling-weights data.
Ethyl calculated adjusted blood-lead values for its principal analysis by
fitting a linear model to adjust for age, sex, race, and income to obtain the
residuals from this analysis. Ethyl did not adjust the individual data for
the effect of the degree of urbanization, a factor recognized to be related to
blood-lead levels. Averages of the adjusted values for 55 of the 64
examination sites were used in the principal (second-stage) analysis.
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ICF used the NHANES II blood leads without adjustnent or transformation.
Adjustment for socio-demographic variables was achieved by including these
variables as covariates in regression models for individual blood leads.
CDC adopted a similar approach, but used the natural logarithms of the NHANES
II blood leads, on the basis of an analysis showing that the distribution of
the values themselves was skewed and that the transformation successfully
corrected for the skewness.
The scale of the dependent variable (raw or logarithm) does not appear to have
a great influence on the final results. With the exception of race, the
blood-lead/gasoline-lead slope in the CDC and ICF analyses appeared stable
across demographic factors, whether the raw or log scale was used for the
dependent variable. The logarithm scale has the advantage of being more
likely to yield normal residuals.
The unit of analysis (factor 3) received a considerable amount of discussion
by reviewers. In particular, the Ethyl two-stage analysis was subjected to
some criticism. At the first stage, the blood lead variable wss adjusted for
differences in the distributions of demographic variables by an indiviudal
level regression on NHANES II data. At the second stage, the adjusted
locality mean blood-lead values were regressed on proxies for gasoline lead
which had not themselves been adjusted for the demographic variables. This
two-step regression procedure leads to bias (see reference 2), but the bias
does not appear important, as Ethyl later corrected the analysis with no
substantial change in the results.
Gasoline Lead Usage/Exposure. There were several different approaches to
defining variables that could be interpreted as indexes of the amount of lead
present in the environment at the time when blood samples were taken, as well
as during the antecedent months. Clearly, no index number or set of index
numbers can serve as an ideal surrogate for a measurement of the exposure
experiences of sampled persons. The Review Group recognizes the complexity of
the mixture of lead sources and uptake pathways.
The large differences between the results of the ICF/CDC analyses and the
Ethyl analysis are caused by different measures of gasoline lead exposure.
ICF and CDC used national period measures-quarterly EPA lead additive data for
CDC and adjusted monthly gasoline sales data for ICF, whereas Ethyl used two
proxy measures for lead exposure at each locality—population density and lead
use per unit area.
A fundamental assumption underlying the creation of a local estimate of
gasoline lead exposure is the notion that the volume of leaded gasoline
consumed locally, with the resulting "fallout", is the primary source of lead
in human blood. Although this determination requires substantive expertise
beyond that on our Review Group, the choice of a local vs. a global measure of
exposure is a pivotal one in all these analyses. If, in fact, lead enters the
human blood system via imported fallout through the food chain (and other
sources), as well as the inhalation of local "fallout", then ideally one would
require a summary measure of exposure which captures both of these sources.
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CDC used data from the quarterly EPA Lead Additive Reports (App. 02, item 14,
pages 37-40 and Appendix H). These are national values of the total amount
(by weight) of lead used in gasoline production. The series exhibits seasonal
fluctuations in gasoline production in addition to a general downward trend.
ICF developed a monthly series of national values of the average amount (by
weight) per day of lead used in gasoline, as follows: Monthly average
gasoline use (liquid volume per day) was obtained from the 00E Monthly Energy
Review. Quarterly values of the concentration of lead in gasoline (grams per
gallon, based on refiner reports) were obtained from EPA (App. 02, item 11).
The product of these produced a monthly series. This series, if aggregated to
a quarterly series, would be closely related to the series used by CDC.
The measures of lead use used by CDC and ICF capture the downward trend in
gasoline lead over time, but they suffer from specification error in that they
are national rather than localized measures of gasoline lead exposure. The
defect has two consequences:
(a.) The gasoline lead use variable does not capture variation in gasoline
lead exposure between localities.
(b.) The lead use variable can be only partially adjusted for correlations
with the demographic covariates.
The COC analysis partially corrects for (a) by aggregating the gasoline lead
exposure over all sampled localites in a six month period of sampling. The
second problem remains, however. The panel does not believe that these
deficiencies invalidate the qualitative findings of a relationship between
lead usage and blood lead. However, the impact on the coefficient of lead
usage in the CDC analysis is not clear.
Ethyl adopted a different approach, seeking to represent gasoline-lead usage
at the survey locations and also to consider separately the effects of lead in
air and lead fallout. The variables used to represent the two kinds of lead
exposure were, respectively, population density and gasoline lead usage per
square mile for the sampled localities.
The Review Group applauded the intention of the Ethyl effort, but the
variables selected appear to be inappropriate. In the Ethyl discussion (App.
02, item 26, Appendix page A-3) it is pointed out that population density is
strongly related to degree of urbanization, a factor for which adjustment is
¦ade in the CDC and ICF analyses, but not in the Ethyl analysis. Furthermore,
Ethyl calculated population density by interpolation between censuses and it
is doubtful that it would reflect changes (if any) in the concentration of
lead in air within the four-year survey period.
Ethyl represented lead usage per unit area by annual values by state.
Department of Transportation reports of annual gasoline sales (by state) and
annual Ethyl estimates of the amount of lead in gasoline being sold (by state)
produced state estimates of annual totals of lead used. These were then
divided by the area of the state. Examination of the resulting values (App.
02, item 26, Table 6, page 23) reveals anomalies. For example, the 1979 lead
usage value for Washington, DC, is 5 times larger than that for any other
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location. The second-largest value 1s the one for New Jersey In 1977, used
for locations adjacent to New York City; it is more than 4 tines the 1977
value used for both New York City and its Westchester County suburbs. As
another example, the computed exposure for Houston, TX (10 no. 28) 1s 101,
compared to 7174 for Washington, DC (ID no. 33). The naive implication of
these two data points 1s that persons living in Washington, DC received a
71-fold (7174/101) increase in dosage of air-lead (or food chain lead)
compared to persons living in Houston, TX. Whether we view this dosage as
exposure through air or food, this extreme differential is highly unlikely.
This variable appears to represent chiefly the statewide average population
density. The Review Group cannot accept it as an indicator of gasoline lead
usage at the sample locations.
Statistical Techniques Used in the Analyses
All final models reported by EPA/ICF and CDC were fitted to the NHANES II data
using the SURREGR procedure available in SAS. This computing software permits
sample weights and cluster design effects to be incorporated into the
variance-covariance estimators of the model parameters. Although unweighted
and weighted ordinary least squares model fitting provided the same
conclusions, SURREGR provides better estimates of standard errors for these
complex survey data. This estimation and hypothesis testing strategy is the
most conservative approach, since it will produce larger standard errors for
the parameter estimates due to the clustering in the data. Extensive
empirical investigations of the role of weights and design effects in the
NHANES I survey demonstrated that test statistics are decreased when Including
weights, and decreased even further when adjusting for design effects (see
reference 3).
The two-stage procedure adopted by Ethyl was described in the preceding
subsection.
Models Used in the Analyses
There is no unique correct approach to analyzing the relationships within the
NHANES II data or between the NHANES II and other data sets. For this reason,
it has been useful to compare and contrast a variety of approaches and models.
All of the models have the general character that a measure of blood lead Is
expressed as a linear combination of a measure (or measure) of exposure to
gasoline lead with various demographic and socioeconomic covariables and
(sometimes) time.
The primary difficulty with the Ethyl analyses (App. 02, item 26) lies in the
choice of constructed gasoline-lead variables. Neither the population density
variable (C19) nor the lead usage variable (C16) is an acceptable measure of
gasoline lead exposure.
The Ethyl report concludes with the observation
In summary, our analysis of the NHANES II data has shown that time
IT) is the major contributor to differences in blood lead between
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1976 and 1980 ... The major contribution of time to the decrease in
blood lead Indicates that other factors that vary with tine are the
major causes of the 1976 to 1980 decrease in blood lead and not
gasoline lead usage.
Ironically, national gasoline lead usage (as defined in the COC or ICF
analysis) 1s such a variable that varies with time and is known to be
causative of some portion of the lead 1n blood. The constructed variable
(C16) does not display a similar relationship with time.
The CDC and ICF/EPA analyses are similar in their general approach. In each
case, a variety of models was considered (adding and deleting various subsets
of the covariables and interaction terms). These variations had only minor
impact on the value of the coefficient for the lead usage variable.
Although both the CDC and EPA/ICF analyses used national data on leaded
gasoline sales, the EPA/ICF models utilized a gasoline lead use variable which
was estimated at each month of the survey (App. D2, item 11, Table 1, pp.
13-14). Consequently, since the data collection period for most of the 64
stands in the NHANES II survey spanned across two months, the gasoline lead
use variable could, and in some cases did, assume two different values for the
same site, according to the month of examination. Investigations of the
relationships between time and blood-lead levels involved comparisons within
sites (due to spanning two months), as well as among sites. Thus, even though
there is a high degree of correlation between time and gasoline lead usage,
these two variables are not completely confounded with the 64 different sites.
It is, nevertheless, a significant question whether the time variable is
included in the model as a covariate. The ICF analysis included a linear time
covariable and seasonal effects in the model, "to give the models the ability
to attribute temporal variations in blood lead to effects other than gasoline
lead" (App. D2, item 11, p. 8). Variables for time and gasoline lead were not
included simultaneously in the CDC analysis.
The intent of the ICF procedure is reasonable, but the confounding between
time and gasoline lead 1n the data make the simultaneous inclusion of these
variables in the model questionable. The data do not allow the relationship
between gasoline lead and blood lead to be estimated at any particular time
point. Thus the attempt to adjust for time is highly dependent on the
specification of the time effects in the model. Despite these problems, two
aspects of the ICF analysis yielded some circumstantial evidence that gasoline
lead is an Important agent of the trend in blood lead. The gasoline lead
variable accounted for seasonal variation 1n blood lead, and the lagged
gasoline lead variables provided a plausible lag structure: the one-month
lagged variable had the strongest association with blood lead.
Gasoline Lead as a Causal Agent for the Decline in Blood-Lead Levels
The CDC and ICF analyses provide strong evidence that gasoline lead is a major
contributor to the decline in blood lead over the period of the NHANES study.
DuPont stressed the limitations of statistical theory and methods as tools for
assessing causal relationships.
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Analysis of the NHANES II data cannot prove whether changes in the use of
leaded gasoline caused a change in average blood-lead levels. Variables X and
Y can be correlated because changes in X cause changes in Y, or vice versa, or
because some third factor, Z, affects both X and Y. There are many other
possibilities as well, but these are enough for this discussion. If X stands
for some measure of average blood lead concentration and Y stands for the
amount of lead in gasoline, we can dismiss the first possibility as absurd.
But the relative plausibility of the other two is a natter for expert
scientific judgement. To date, no hypothesis of the third form which could
explain the NHANES II data has been presented to the panel. One hypothesis of
this form has been discussed. This hypothesis has Z representing regulatory
changes and publicity aimed at reducing lead exposure generally. This could
result in reductions in gas lead, lead in food, lead in paint, etc., and it
could be that the gas lead change had little effect on blood-lead levels --
the blood-lead changes might have been caused by the other factors (food,
paint, etc.). Although this hypothesis cannot be disregarded entirely, it
does not seem to explain the blood-lead drop adequately. We have seen little
evidence that food lead has dropped by a factor large enough to explain a
sizable part of the drop in blood lead. In fact, the FDA diet lead values
shown in the ICF Report (App- D2, item 11, Table 2) were increasing during the
study period. That changes in exposure to leaded paint caused the decrease in
blood-lead observed over all age and sex groups seems highly unlikely. The
existence of influences (other than gasoline lead usage) that are not included
in the models must be recognized as a limiting factor in the evaluation of all
of the analyses.
Use of NHANES II Data for Forecasting Results of Alternative Regulatory Policies
Regression models have been used in all three analyses to see if the NHANES II
time trend in average blood-lead levels can be explained in terms of changes
in demographic variables or in terms of changes in gas and lead usage.
Extension of the use of these and other statistical techniques "to estimate
the distribution of blood-lead levels of whites, blacks, and black children
and to forecast the results of alternative regulations," as in Section III of
the ICF Report of December, 1982 (App. D2, item 11), raises questions and
involves assumptions that go much further than those the Review Group was able
to consider. In general, the Review Group would warn that the weaknesses that
have been discussed in the context of analyzing relationships within the
four-year survey period become enormously greater in any attempt to
extrapolate beyond that period. For example, the cautions mentioned in the
IRC review (App. D2, item 22, p. 6) of the ICF analysis probably do not go far
enough.
Summary
In general, there is a significant correlation between gasoline-lead levels
and blood-lead levels in persons examined in the NHANES II Survey. Major
obstacles interfere with the use of the available data to describe the
relationship. They are: the need to perform model-based adjustments to
compensate for imbalance in the design of the NHANES II, the possibility of
specification error in the regression models, and the lack of a satisfactory
measure of individual or local exposure to gasoline lead, in addition to
sampling error, laboratory measurement error, and the high nonresponse rate.
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The Review Group finds that the Ethyl analyses contribute little to
understanding the association between blood lead and gasoline lead because the
variables adopted to represent lead exposure are deemed inappropriate.
The CDC and ICF/EPA analyses relating the NHANES II blood-lead data to a
national measure of the aaount of lead used in gasoline indicate that the drop
in average blood-lead levels can be explained, in large part, by the
concurrent drop in gasoline lead. This by no neans confirms the hypothesis
that the blood lead decrease was caused by the decrease In gasoline lead but,
in the absence of scientifically plausible alternative explanations, that
hypothesis Bust receive serious consideration.
References
Literature cited in this report, In addition to the documents furnished by the
EPA which are listed in Appendix D2.
(1) Ling, R. F. (1982). A review of Correlation and Causation by David A. Kenny,
John Wiley & Sons. J. Am. Statis. Assoc. 77. 115-491.
(2) Goldberger, A. S. (1961). Step wise Least Squares: Residual Analysis and
Specification Error. J. Am. Statis. Assoc. 56, 998-1000.
(3) Landis, J. R., LepkowsM, J. M., Eklund, S. A. and Stehouwer, S. A. (1982).
A General Methodolody for the Analysis of Data from the NHANES I Survey.
Vital and Health Statistics. NCHS Series 2- No. 92. DHHS Pub! No. (PHS)
82-13657" Washington.U.S. Government PrTnlfng~Sffice.
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Appendix 01
Questions for the Review Group
The following questions were stated 1n letters to members of the Review Group
from Dr. Lester D. Grant, Director of the EPA Environmental Criteria and
Assessment Office, February 17, 1983.
1. To what extent is it valid to use the NHANES II data to determine time
trends for changes in nationally representative blood-lead values for the
years of the study (1976-1980)? More specifically, to what extent can the
NHANES II data appropriately be used to define time trends for blood-lead
levels (aggregated on an annual, semiannual, or any other time-related basis)
for the total NHANES II sample (all ages, sexes, races, etc.) or for
subsamples defined by the following demographic variables: (1) age (e.g.,
children <6 years old, children 6-12 years old, adults by 10- or 20- year age
groups); (2) sex; (3) race; (4) geographic location (e.g., urban vs. rural
residence; Northeast vs. Southeast, Midwest, or other large regional areas of
the U.S.; residence in specific cities, towns, or rural locales); (5)
socioeconomic status; (6) occupation of respondants or their parents/head of
household at main residence; or (7) any combination of such demographic
variables (e.g., black children <6 years or white children <6 years old living
in urban or rural areas, etc.).
2. If it is indeed possible to derive such time trends from the NHANES II
data, to what extent can the changes 1n NHANES II blood-lead levels over time
be correlated credibly with changes In the usage of leaded gasoline over the
same time period (i.e., the years 1976-1980)? Several analyses of this type
have already been conducted and submitted to us, and we would appreciate your
evaluation of those analyses.
3. Are there any other appropriate credible statistical approaches or
analyses, besides those alluded to as already having been done, that might be
carried out with the NHANES II data to evaluate relationships over time
between blood-lead levels and gasoline lead usage?
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Appendix 02
Documents Considered by
NHANES II TIME TREND ANALYSIS REVIEW GROUP
1. Plan and Operation of the Second National Health and Nutrition Examina-
tion Survey. (1976-1980) National Center for Health Statistics, Series 1,
No. 15. July, 1981.
2. Public Use Data Tape Documentation. Hematology and Biochemistry, catalog
number 5411. NHANES II Survey, 1976-1980, NCHS. July, 1982.
3. NHANES II Weight Deck (one record for each SP). Deck #502. Attachment
I, NCHS.
4. NHANES II Sampling Areas. Document furnished by NCHS during site visit,
March 10, 1983.
5. Steps in Selection of PSU's for the NHANES II Survey. Document furnished
by NCHS during site visit, March 10, 1983.
6. Location of Primary Sampling Units (PSU) chronologically by pair of cara-
vans: NHANES II Survey, 1976-80. Document"furnished by NCHS during site
visit, March 10, 1983.
7. Annest, J. L. et al, (1982) Blood lead levels for person 6 months - 74
years of age: United States, 1976-1980. NCHS ADVANCEDATA, No. 79, May 12,
1982.
8. Mahaffey, K. R. et al. (1982) National estimates of blood lead levels:
United States, 1976-1980. Association with selected demographic and socio-
economic factors. New England Journal of Medicine 307: 573-579.
9. Average Blood Lead Levels for White Persons, 6 months - 74 years strat-
ified chronologically by PSU's: NHANES II, 1976-80 by caravan. "Graph"
furnished by NCHS, March 17, 1983.
10. Schwartz, J. The use of NHANES II to investigate the relationship between
gasoline lead and blood lead. Memo to David Weil (ECAO) (March 3, 1983).
11. ICF Report: The Relationship between Gasoline Lead Usage and Blood Lead
Levels in Americans: A Statistical Analysis of the NHANES II Data.
December 1982.
12. Annest, J. L. et al. (1983) The NHANES II study. Analytic error and its
effect on national estimates of blood lead levels.
13. Pirkle, J. L. Comments on the Ethyl Corp. analysis of the NHANES II data
submitted to EPA October 8, 1982 (Feb. 26, 1983).
14. Pirkle, J. L. Chronological trend in blood lead levels of the second
NHANES, Feb. 1976-Feb. 1980 (Feb. 26, 1983).
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15. Lynam, D. R. Letter to David Weil dated October 15, 1982 containing ad-
ditional comments on NHANES II data.
16. E. I. DuPont de Nemours & Co., Inc. Supplementary statement presented to
EPA in the matter of regulation of fuel and fuel additives - lead phase-
down regulations proposed rulemaking (Oct. 8, 1982).
17. Pirkle, J. L. An expanded regression model of the NHANES II blood lead
data including more than 100 variables to explain the downward trend from
Feb., 1976-Feb., 1980 (Dec, 23, 1982).
18. Annest, J. L. et al. Table 1. Average blood lead levels and total non-
response rates for persons ages 6 months - 74 years stratified chrono-
logically by primary sampling unit (PSU): NHANES II, 1976-1980 (Corrected
version; April 8, 1983).
19. Pirkle, J. L. (1983). Duplicate measurements differing by more than 7
mg/dl in the lead measurements done in NHANES II Survey. Document fur-
nished by CDC at Panels request, March 18, 1983.
20. Pirkle, J. I. Appendix M: Tabulation by demographic variables (March 18,
1983).
21. Pirkle, J. t. Appendix N: Regression analysis of urban and rural popu-
lation subgroups (March 18, 1983).
22. Miller, C. and Violette, D. Comments on studies using the NHANES II data
to relate human blood lead levels to lead use as a gasoline additive
(March, 1983).
23. Miller, C. and Violette, D. (March 4, 1983). The Usefulness of the
NHANES II Data for Discerning the Relationship between Gasoline Lead
Levels and Blood Lead Levels in Americans and a Review of ICF's Analysis
using the NHANES II Data. Energy and Resource Consultants, Inc.;
Boulder, Colorado.
24. Schwartz, J. Analysis of NHANES II data to determine the relationship be-
tween gasoline lead and blood lead. Memo to David Weil (ECA0). (March
18, 1983).
25. Excerpt - (Section I. C. - "Discussion of NHANES II Blood Lead Data")
from the Ethyl submission to the EPA's docket on the Lead Phasedown dated
Hay 14, 1982.
26. Excerpt - (Section III. A. - entitled "Correlation of Blood Lead to Gaso-
line Lead" and Appendix "Discrete Linear Regression Study") from the
Ethyl submission to EPA's docket on the Lead Phasedown. (October 8, 1982)
27. Ethyl Analyses of the NHANES II Data. This item was distributed at the
Criteria Document meeting held on January 18-20, 1983.
28. Comments by Dr. Norman R. Draper on Ethyl Corporation's comments and ICF,
Inc.'s comments.
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23. Comments by Dr. Ralph A. Bradley entitled "A Discussion of Issues and
Conclusions on Gasoline Lead Use and Hunan Blood Lead Levels".
30. Comments by Dr. Ralph A. Bradley in a letter to B. F. Fort. (Ethyl Corp.)
31. Ethyl Corp. NHANES II - blood lead data correlation with air lead concen-
tration data.
32. Ethyl Corp. Summary of analyses of the NHANES II blood lead data (Janu-
ary, 1983).
33. E. I. DuPont de Nemours & Co, Comments submitted March 21, 1983.
34. E. I. DuPont de Nemours & Co. Comments by R. Snee and C. Pfieffer on
paper by Annest et al. on analytic error (see item #5).
35. Pirkle, J. L. The relationship between EPA air lead levels and population
density. (March, 1983),
36. Pirkle, J. Consecutive numbering of points on plots of 6-month average
NHANES II blood lead levels versus 6-month total lead used in gasoline
(April 11, 1983).
37. Pirkle, J. L. Distribution of the NHANES II lead subsample "weight" vari-
able (April 11, 1983).
38. Pirkle, J. L. Appendix 0: Propagation of error in calculating the percent
decrease in blood lead levels over the NHANES II survey period (April 11,
1983).
39. Pirkle, J. L. Appendix P: Regressing In (blood lead) on the demographic
covariates and then regressing the residuals on GASQ compared to regres-
sing In (blood lead) simultaneously on the demographic covariates + GASQ
(April 11, 1983).
40. Pirkle, J. L. Appendix Q: Regression of In (blood lead) on the demo-
graphic covariates only and subsequently adding GASQ: F statistics, R
square and Mallows C (p) (April 11, 1983).
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Appendix D3
List of Attendees at March 10-11 and March 30-31, 1983
meeting of
NKANES II TIME TREND ANALYSIS REVIEW GROUP
Panel Members
Joan Rosenblatt (Chairaan)
National Bureau of Standards
J, Richard Landis
University of Michigan
Roderick Little
Bureau of the Census
Richard Royal1
Johns Hopkins University
Harry Smith, Jr.
Mt. Sinai School of Medicine
David Weil (Co-chairman)
U.S. EPA
Observers
Dennis Kotchmar*
U.S. EPA
Vic Hasselblad
U.S. EPA
Allen Marcus
U.S. EPA
Robert Murphy
NCHS
Vernon Houkt
Centers for
James Pirkle
Centers for
Disease Control
Disease Control
George Provenzano
U.S. EPA
Joel Schwartz
U.S. EPA
Earl Bryant*
NCHS
Trena Ezzote*
NCHS
J. Lee Annest
NCHS
Mary Kovar*
NCHS
Bob Casady*
NCHS
Jean Roberts*
NCHS
Don tynam
Ethyl Corporation
Ben Forte
Ethyl Corporation
Jack Pierrard*
DuPont
Chuck Pfieffer
DuPont
Ron Snee
DuPont
Asa Janney
ICF
Kathryn Mahaffey*
FDA
•attended March 10-11 meeting only,
tattended March 30-31 meeting only.
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